Systems for stimulation of effector tissue

Abstract

A system for treating erectile dysfunction in a male person is disclosed. The system comprises a stimulation device configured to deliver, directly or indirectly: a first stimulation signal to a sympathetic nerve innervating a penile vein of the person; and a second stimulation signal to a parasympathetic nerve innervating a penile artery of the person. The system further comprises a control unit configured to control an operation of the stimulation device such that: the first stimulation signal stimulates an activity of the sympathetic nerve, thereby causing vasoconstriction of the penile vein; and the second stimulation signal stimulates an activity of the parasympathetic nerve, thereby causing vasodilation of the penile artery. The vasodilation of the penile artery increases a blood flow entering an erectile body of the penis and the vasoconstriction of the penile vein reduces a blood flow exiting the erectile body, thereby inducing engorgement of the erectile body.

Description

[0001]SYSTEMS AND METHODS FOR STIMULATION OF EFFECTOR TISSUE Technical field The present disclosure relates to systems and methods for stimulation of effector tissue in the human body. Background The nervous system of the body innervates various types of tissue, which may be commonly referred to as effector tissue. Generally, effector tissue may be understood as tissue that produce a response or perform work (‘effector response’) when activated by nerve signals. Examples include muscles (skeletal muscles, smooth muscle) and glands (endocrine glands and exocrine glands). They may furthermore be categorized based on their relationship with the nervous system. The somatic effectors are mostly skeletal muscles controlled by the somatic nervous system, responsible for voluntary actions, whereas the autonomic effectors typically are controlled by the autonomic nervous system and include smooth muscle tissue, cardiac muscle, and glands. These effectors are generally not under voluntary control. The sympathetic nervous system (SNS) and the parasympathehtic nervous system (PNS) form the autonomous nervous system and may have complementary functions on the same effector tissue, such as an organ or a muscle. For example, the SNS may accelerate the heart rate, while the PNS may slow it down. Both the SNS and the PNS are typically active to some extent all the time, but their relative activities may change depending on the situation. This dynamic balance between the SNS and the PNS is commonly referred to as the “autonomic tone”. The autonomic tone hence implies there is an ongoing, background level of activity in the SNS and PNS. The body may adjust this balance as needed, ramping up sympathetic or parasympathetic activity in response to specific situations. The tone may also capture the systems’ readiness to respond to stimuli. A certain “tone” or baseline activity level may ensure that the system can quickly ramp up or down its activity to adapt to different situations. The nervous system of the body regulates and affects a great variety of bodily functions, and it is therefore of interest to control or modulate various parts of the nervous system for therapeutic purposes, such as for treating obesity, affecting sexual dysfunction, and adjusting the blood pressure. Summary It is an object of the present invention to provide improved technologies and methods for affecting an effector response in a human body. According to an embodiment, a system for treating erectile dysfunction in a male person is disclosed. The system comprises a stimulation device configured to deliver, directly or indirectly: a first stimulation signal to a sympathetic nerve innervating a penile vein of the person; and a second stimulation signal to a parasympathetic nerve innervating a penile artery of the person. The system further comprises a control unit configured to control an operation of the stimulation device such that: the first stimulation signal stimulates an activity of the sympathetic nerve, thereby causing vasoconstriction of the penile vein; and the second stimulation signal stimulates an activity of the parasympathetic nerve, thereby causing vasodilation of the penile artery. The vasodilation of the penile artery increases a blood flow entering an erectile body of the penis and the vasoconstriction of the penile vein reduces a blood flow exiting the erectile body, thereby inducing engorgement of the erectile body. According to an embodiment, a system for affecting an effector response in a patient is provided. The system comprises a stimulation device configured to deliver, directly or indirectly, a first stimulation signal to a sympathetic nerve innervating a first effector tissue of the patient, and a second stimulation signal to a parasympathetic nerve innervating a second effector tissue. The system further comprises a control unit configured to control an operation of the stimulation device such that: the first stimulation signal stimulates an activity of the sympathetic nerve and the second stimulation signal inhibits an activity of the parasympathetic nerve, or the first stimulation signal inhibits an activity of the sympathetic nerve and the second stimulation signal stimulates an activity of the parasympathetic nerve. In an example, the control unit may be configured to control the operation of the stimulation device such that at least one of the first stimulation signal and the second stimulation signal is a periodic signal including at least one of: a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component. In an example, the first signal may be a low-frequency signal configured to stimulate the activity of the sympathetic nerve and the second signal is a high-frequency signal configured to inhibit the activity of the parasympathetic nerve. Alternatively, the first signal may be a high-frequency signal configured to inhibit the activity of the sympathetic nerve and the second signal is a low-frequency signal configured to stimulate the activity of the parasympathetic nerve. In an example, an amplitude of the low-frequency signal may vary with a frequency in the range of 0.1 - 100 Hz and an amplitude of the high-frequency signal vary with a frequency in the range of 1 - 10 kHz. In an example, at least one of the first and second stimulation signals may comprise a series of pulses having a negative voltage relative to ground. In an example, the control unit may be configured to operate the stimulation device to generate a positive voltage pulse following one or more negative voltage pulses. In an example, at least one of the first stimulation signal and second stimulation signal may be an electric signal or a vibrational signal. In an example, the control unit may be configured to operate the stimulation device to alternatingly apply the first stimulation signal to the sympathetic nerve and the second stimulation signal to the parasympathetic nerve. In an example, the control unit may be configured to operate the stimulation device to simultaneously apply the first stimulation signal to the sympathetic nerve and the second stimulation signal to the parasympathetic nerve. In an example, the control unit may be configured to control the operation of the stimulation device to generate an effector response being at least one of a muscular response and a glandular response. In an example, each of the first and second effector tissue may be a muscular tissue. Further, the control unit may be configured to control the operation of the stimulation device such that the first stimulation signal stimulates the activity of the sympathetic nerve and the second stimulation signal inhibits the activity of the parasympathetic nerve, thereby inducing contraction in the muscular tissue. In an example, each of the first and second effector tissue may be a muscular tissue. Furthermore, the control unit may be configured to control the operation of the stimulation device such that the first stimulation signal inhibits the activity of the sympathetic nerve and the second stimulation signal stimulates the activity of the parasympathetic nerve, thereby inducing relaxation in the muscular tissue. In an example, the first and second effector tissue may be smooth muscle tissue. In an example, the first and second effector tissue may form part of a blood vessel, an intestine, or a urine bladder of the patient. In an example, the system may further comprise a sensor device configured to generate a sensor signal indicating an effector response in the effector tissue and a control unit configured to receive the sensor signal and control an operation of the stimulation device based at least in part on the sensor signal. In an example, the sensor device may comprise a sensor electrode configured to measure an electric activity in the effector tissue. In an example, the sensor device may comprise a sensor electrode configured to measure a change in electrical impedance in the effector tissue. In an example, the sensor device may comprise an electromyographic sensor configured to measure an electric activity in the effector tissue and an electric impedance sensor configured to measure a change in electrical impedance in the effector tissue. In an example, the sensor electrode may be configured to be arranged at the effector tissue. The sensor may further comprise a reference electrode and be configured to generate the sensor signal based on an electrical interaction between the sensor electrode and the reference electrode. In an example, the reference electrode may be formed by a housing of the stimulation device or the sensor device. In an example, the sensor device may be configured to measure mechanical movement in the effector tissue. In an example, the sensor device may comprise a strain gauge configured to measure a contraction or relaxation of the effector tissue. In an example, the control unit may be configured to determine a response measure based on the sensor signal, the response measure being indicative of the effector response. In an example, the control unit may be configured to compare the response measure with a predetermined reference measure and control the stimulation device to, in response to the response measure being below the reference measure, increase an intensity of the first stimulation signal to stimulate the activity in the sympathetic nerve and / or increase an intensity of the second stimulation signal to inhibit the activity of the parasympathetic nerve. Further, the control unit may be configured to control the stimulation device to, in response to the response measure exceeding the reference measure, reduce the intensity of the first stimulation signal to inhibit the activity of the sympathetic nerve and / or stimulate the activity of the parasympathetic nerve. The predetermined reference measure may be based on a previous measurement of the effector response in the patient or previous measurement of effector responses in other patients. In an example, the control unit may be configured to monitor the response measure of the effector response over time, and to control the stimulation device based on a change rate in the effector response over time. In an example, the control unit may be configured to determine a calibration parameter of the stimulation device based on the response measure. In an example, the stimulation device may comprise a first electrode arrangement configured to be coupled to the sympathetic nerve to deliver the first stimulation signal and a second electrode arrangement configured to be coupled to the parasympathetic nerve to deliver the second stimulation signal. In an example, the first electrode arrangement may comprise a first stimulation electrode and a second stimulation electrode, wherein the first stimulation electrode and the second stimulation electrode may be configured to be spaced apart along the sympathetic nerve. In an example, the stimulation device may be configured to generate the first stimulation signal such that the first stimulation electrode serves as a cathode and the second stimulation electrode serves as an anode. In an example, the system may further comprise a cuff configured to be at least partially arranged around the nerve and hold the first electrode arrangement in place against the sympathetic nerve. In an example, the second electrode arrangement may comprise a third electrode and a fourth electrode, wherein the third electrode and the fourth electrode are configured to be arranged spaced apart along the parasympathetic nerve. The second electrode arrangement may further comprise a fifth electrode configured to be arranged spaced apart from the fourth electrode such that the fourth electrode is arranged between the third and fifth electrodes. In an example, the stimulation device may be configured to generate the second stimulation signal such that the fourth electrode serves as a cathode and the third and fifth electrodes serve as anodes. In an example, the system may further comprise a cuff configured to be at least partially arranged around the parasympathetic nerve and hold the second electrode arrangement in place against the parasympathetic nerve. According to an embodiment, a system for affecting an effector response in a patient is provided, comprising a stimulation device configured to be coupled to at least one of an effector tissue and a nerve innervating the effector tissue of the patient, and a control unit configured to operate the stimulation device to apply at least one of a first stimulation signal and a second stimulation signal to the effector tissue. The first stimulation signal is a time-varying signal with an amplitude varying with a frequency lying in a first frequency interval and the second stimulation signal is a time-varying signal with an amplitude varying with a frequency lying in a second frequency interval. The first frequency interval is selected to inducing the effector response in the effector tissue and the second frequency interval is selected to inhibit the effector response in the effector tissue. In an example, the first frequency interval may be 0.1 - 100 Hz and the second frequency interval 1 - 10 kHz. In an example, at least one of the first and second stimulation signals may be an electric signal comprising a series of pulses having a negative voltage relative to ground. In an example, the control unit may be configured to operate the stimulation device to generate a positive voltage pulse following one or more negative voltage pulses. In an example, the control unit may be configured to operate the stimulation device to generate a first stimulation signal having a frequency of 0.5 - 3 Hz, and wherein the effector tissue is cardiac muscle tissue. In an example, the control unit may be configured to operate the stimulation device to generate a first stimulation signal having a frequency of 1 - 10 Hz, and wherein the effector tissue is skeletal muscle tissue. In an example, the control unit may be configured to operate the stimulation device to generate a first stimulation signal having a frequency of 0.1 - 100 Hz, and wherein the effector tissue is smooth muscle tissue. In an example, at least one of the first stimulation signal and second stimulation signal may be an electric signal or a vibrational signal. In an example, the control unit may be configured to operate the stimulation device to alternatingly apply the first stimulation signal and the second stimulation signal to the effector tissue. In an example, the system may further comprise a sensor device configured to generate a sensor signal indicating an effector response in the effector tissue, wherein the control unit may be configured to receive the sensor signal and control an operation of the stimulation device based at least in part on the sensor signal. In an example, the sensor device may comprise a sensor electrode configured to measure an electric activity in the effector tissue. In an example, the sensor device may comprise a sensor electrode configured to measure a change in electrical impedance in the effector tissue. In an example, the sensor device may comprise an electromyographic sensor electrode configured to measure an electric activity in the effector tissue and an electric impedance sensor electrode configured to measure a change in electrical impedance in the effector tissue. In an example, the sensor electrode may be configured to be arranged at the effector tissue. The sensor may further comprise a reference electrode and be configured to generate the sensor signal based on an electrical interaction between the sensor electrode and the reference electrode. In an example, the reference electrode may be formed by a housing of the stimulation device or the sensor device. In an example, the sensor device may be configured to measure mechanical movement in the effector tissue. In an example, the sensor device may comprise a strain gauge configured to measure a contraction or relaxation of the effector tissue. In an example, the control unit may be configured to determine a response measure based on the sensor signal, the response measure being indicative of the effector response. In an example, the control unit may be configured to compare the response measure with a predetermined reference measure and control the stimulation device to: in response to the response measure being below the reference measure, increase an intensity of the first stimulation signal to stimulate the activity in the effector tissue, and in response to the response measure exceeding the reference measure, increase the intensity of the second stimulation signal to inhibit the activity of the effector tissue. The predetermined reference measure may be based on a previous measurement of the effector response in the patient or previous measurement of effector responses in other patients. In an example, the control unit may be configured to monitor the response measure of effector response over time and control the stimulation device based on a change rate in the effector response over time. In an example, the control unit may be configured to determine a calibration parameter of the stimulation device based on the response measure. In an example, the stimulation device may comprise a first electrode arrangement configured to deliver the first stimulation signal and a second electrode arrangement configured to deliver the second stimulation signal. The first electrode arrangement may comprise a first stimulation electrode and a second stimulation electrode, wherein the first stimulation electrode and the second stimulation electrode are configured to be spaced apart along the nerve innervating the effector tissue. In an example, the stimulation device may be configured to generate the first stimulation signal such that the first stimulation electrode serves as a cathode and the second stimulation electrode serves as an anode. In an example, the system may further comprise a cuff configured to be at least partially arranged around the nerve and hold the first electrode arrangement in place against the nerve. In an example, the second electrode arrangement may comprise a third electrode and a fourth electrode, the third electrode and the fourth electrode being configured to be arranged spaced apart along the nerve. In an example, the stimulation device may be configured to generate the second stimulation signal such that the third electrode serves as a cathode and the fourth electrode serves as an anode. In an example, the system may further comprise a cuff configured to be at least partially arranged around the nerve and hold the second electrode arrangement in place against the nerve. In an example, the system may further comprise a suppression electrode arrangement configured to be coupled to the nerve to apply a suppression signal suppressing action potentials propagating in the nerve in a direction towards the central nervous system. In an example, the control unit may be configured to regulate the suppression signal so as to suppress the action potentials induced in response to the stimulation device applying the first stimulation signal. In an example, the stimulation device may be configured to be coupled to the nerve at a position between the effector tissue and the suppression electrode arrangement, so as to induce action potentials travelling in the nerve in a direction towards the effector tissue. In an example, the control unit may be configured to regulate the suppression of the action potentials so as to inhibit an undesired response of the nervous system of the patient, the undesired response being generated responsive to the stimulation device applying the first stimulation signal. In an example, the control unit may be configured to drive the stimulation device and the suppression electrode arrangement such that each of the stimulation device and the suppression electrode arrangement is actuated in sequence, with a delay of the suppression signal timed to generally match a conduction velocity of the first stimulation signal. In an example, the control unit may be configured to drive the stimulation device and the suppression electrode arrangement to apply the first stimulation signal and the suppression signal substantially at the same time. In an example, the control unit may be configured to drive the stimulation device and the suppression electrode arrangement such that each of the first stimulation signal and the suppression signal is a time-varying signal, wherein the first stimulation signal is a low-frequency signal, and the suppression signal is a high-frequency signal. An amplitude of the first stimulation signal may vary with a frequency in the range of 0.1 - 100 Hz, while an amplitude of the suppression signal may vary with a frequency in the range of 1 - 10 kHz. According to an embodiment, a system for affecting an effector response in a patient is provided. The system comprises a stimulation device comprising a first and a second electrode arrangement, wherein each is configured to be coupled to at least one of an effector tissue and a nerve innervating the effector tissue of the patient, and a control unit configured to drive the stimulation device to apply, by means of the first electrode arrangement, a stimulation signal inducing the effector response in the effector tissue and apply, by means of the second electrode arrangement, a suppression signal suppressing action potentials propagating in the nerve towards the central nervous system (CNS). The control unit is configured to regulate the suppression signal so as to suppress the action potentials induced in response to the stimulation device applying the stimulation signal. In an example, the first electrode arrangement may be configured to be coupled to the nerve at a position between the effector tissue and the second electrode so as to induce action potentials travelling in the nerve in a direction towards the effector tissue. In an example, the control unit may be configured to regulate the suppression of the action potentials so as to inhibit an undesired response of the nervous system of the patient, the undesired response being generated responsive to the first electrode applying the stimulation signal. In an example, the control unit may be configured to drive the stimulation device such that each of the first and second electrode arrangements are actuated in sequence, with a delay of the suppression signal timed to generally match a conduction velocity of the stimulation signal. In an example, the control unit may be configured to drive the stimulation device to apply the stimulation signal and the suppression signal substantially at the same time. In an example, the control unit may be configured to drive the stimulation device such that each of the stimulation signal and the suppression signal is a time-varying signal, wherein the stimulation signal is a low-frequency signal and the suppression signal is a high- frequency signal. An amplitude of the stimulation signal may vary with a frequency in the range of 0.1 - 100 Hz, while an amplitude of the suppression signal may vary with a frequency in the range of 1 - 10 kHz. In an example, the first and second electrode arrangements may be configured to be spaced apart along nerve. In an example, the first electrode arrangement may comprise a first stimulation electrode and a second stimulation electrode configured to apply the stimulation signal to the effector tissue or nerve. In an example, the first stimulation electrode and the second stimulation electrode may be configured to be spaced apart along the nerve. In an example, the stimulation device may be configured to generate the stimulation signal such that the first stimulation electrode serves as a cathode and the second stimulation electrode serves as an anode. In an example, the system may further comprise a cuff configured to be at least partially arranged around the nerve and hold the first electrode arrangement in place against the nerve. In an example, the second electrode arrangement may comprise a first suppression electrode and a second suppression electrode configured to apply the suppression signal to the nerve. In an example, the first suppression electrode and the second suppression electrode may be configured to be spaced apart along the nerve. In an example, the second electrode arrangement may further comprise a third suppression electrode configured to be arranged spaced apart from the second suppression electrode such that the second suppression electrode is arranged between the first and third suppression electrodes. In an example, the stimulation device may be configured to generate the suppression signal such that the second suppression electrode serves as a cathode and the first and third suppression electrodes serve as anodes. In an example, the system may further comprise a cuff configured to be at least partially arranged around the nerve and hold the second electrode arrangement in place against the nerve. In an example, the system may further comprise a sensor device configured to generate a sensor signal indicating an effector response in the effector tissue. The control unit may be further configured to receive the sensor signal and control an operation of the stimulation device based at least in part on the sensor signal. In an example, the sensor device may comprise a sensor electrode configured to measure an electric activity in the effector tissue. In an example, the sensor device may comprise a sensor electrode configured to measure a change in electrical impedance in the effector tissue. In an example, the sensor device may comprise an electromyographic sensor electrode configured to measure an electric activity in the effector tissue and an electric impedance sensor electrode configured to measure a change in electrical impedance in the effector tissue. In an example, the sensor electrode may be configured to be arranged at the effector tissue. The sensor may further comprise a reference electrode and be configured to generate the sensor signal based on an electrical interaction between the sensor electrode and the reference electrode. In an example, the reference electrode may be formed by a housing of the stimulation device or the sensor device. In an example, the sensor device may be configured to measure mechanical movement in the effector tissue. The sensor device may comprise a strain gauge configured to measure a contraction or relaxation of the effector tissue. In an example, the control unit may be configured to determine a response measure based on the sensor signal, the response measure being indicative of the effector response. The control unit may be configured to compare the response measure with a predetermined reference measure and control the stimulation device to: in response to the response measure being below the reference measure, increase an intensity of the stimulation signal to stimulate the activity in the effector tissue, and in response to the response measure exceeding the reference measure, reduce the intensity of the stimulation signal to inhibit the activity of the effector tissue. The predetermined reference measure may be based on a previous measurement of the effector response in the patient or previous measurement of effector responses in other patients. In an example, the control unit may be configured to monitor the response measure of the effector response over time and control the stimulation device based on a change rate in the effector response over time. In an example, the control unit may be configured to determine a calibration parameter of the stimulation device based on the response measure. According to an embodiment, a system for affecting an effector response in a patient is provided, comprising a stimulation device configured to deliver, directly or indirectly, a stimulation signal to at least one of an effector tissue and a nerve innervating the effector tissue of the patient, a sensor device configured to generate a sensor signal indicating an effector response in the effector tissue, and a control unit. The control unit is configured to receive the sensor signal and control an operation of the stimulation device based at least in part on the sensor signal. In an example, the sensor device may comprise a sensor electrode configured to measure an electric activity in the effector tissue in response to the stimulation signal. In an example, the sensor device may comprise a sensor electrode configured to measure a change in electrical impedance in the effector tissue in response to the stimulation signal. In an example, the sensor device may comprise an electromyographic sensor configured to measure an electric activity in the effector tissue and an electric impedance sensor configured to measure a change in electrical impedance in the effector tissue. In an example, the sensor electrode may be configured to be arranged at the effector tissue. The sensor electrode may comprise a reference electrode and the sensor device may be configured to generate the sensor signal based on an electrical interaction between the sensor electrode and the reference electrode. The reference electrode may be formed by a housing of the stimulation device or the sensor device. In an example, the sensor device may be configured to measure mechanical movement in the effector tissue in response to the stimulation signal. The sensor device may comprise a strain gauge configured to measure a contraction or relaxation of the effector tissue in response to the stimulation signal. In some examples, the sensor device may be configured to measure a heart rate of the patient, a blood pressure of the patient, or a rate of respiration of the patient. In an example, the control unit may be configured to determine a response measure based on the sensor signal, the response measure being indicative of the effector response. In an example, the control unit may be configured to compare the response measure with a predetermined reference measure and control the stimulation device to: increase an intensity of the stimulation signal in response to the response measure being below the reference measure, and reduce the intensity of the stimulation signal in response to the response measure exceeding the reference measure. In an example, the control unit may be configured to increase the intensity of the stimulation signal by increasing at least one of a frequency, current amplitude and voltage amplitude of the stimulation signal and reduce the intensity of the stimulation signal by reducing at least one of the frequency, current amplitude and voltage amplitude of the stimulation signal. The predetermined reference measure may be based on a previous measurement of the effector response in the patient or previous measurement of effector responses in other patients. In an example, the control unit may be configured to monitor the level of effector response over time and control the stimulation device based on a change rate in the effector response over time. In an example, the control unit may be configured to determine a calibration parameter of the stimulation device based on the response measure. In an example, the control unit may be configured to control the operation of the stimulation device to generate an effector response being at least one of a muscular response and a glandular response. The effector tissue may be smooth muscle tissue, such as forming part of a blood vessel, an intestine, or a urine bladder of the patient. In an example, the control unit may be configured to control the operation of the stimulation device such that the stimulation signal is a periodic signal including at least one of: a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component. The stimulation signal may be one of a low-frequency signal with an amplitude varying in the range of 0.1 - 100 Hz and a high-frequency signal with an amplitude varying in the range of 1 - 10 kHz. The stimulation signal may comprise series of pulses having a negative voltage relative to ground. In an example, the control unit may be configured to operate the stimulation device to generate a positive voltage pulse following one or more negative voltage pulses. The stimulation signal may be an electric signal or a vibrational signal. In an example, the stimulation device may comprise a first stimulation electrode and a second stimulation electrode, the first stimulation electrode and the second stimulation electrode being configured to be spaced apart along the nerve innervating the effector tissue. The stimulation device may be configured to generate the stimulation signal such that the first stimulation electrode serves as a cathode and the second stimulation electrode serves as an anode. The system may further comprise a cuff configured to be at least partially arranged around the nerve and hold the first and second stimulation electrodes in place against the nerve. In an example, the system may further comprise a suppression electrode arrangement configured to be coupled to the nerve to apply a suppression signal suppressing action potentials propagating in the nerve in a direction towards the central nervous system. The control unit may be configured to regulate the suppression signal so as to suppress the action potentials induced in response to the stimulation device applying the stimulation signal. Furthermore, the stimulation device may be configured to be coupled to the nerve at a position between the effector tissue and the suppression electrode arrangement, so as to induce action potentials travelling in the nerve in a direction towards the effector tissue. In an example, the control unit may be configured to regulate the suppression of the action potentials so as to inhibit an undesired response of the nervous system of the patient, the undesired response being generated responsive to the stimulation device applying the stimulation signal. In an example, the control unit may be configured to drive the stimulation device and the suppression electrode arrangement such that each of the stimulation device and suppression electrode arrangement is actuated in sequence, with a delay of the suppression signal timed to generally match a conduction velocity of the stimulation signal in the nerve. In an example, the control unit may be configured to drive the stimulation device and the suppression electrode arrangement to apply the first stimulation signal and the suppression signal substantially at the same time. In an example, the control unit may be configured to drive the stimulation device and the suppression electrode arrangement such that each of the stimulation signal and the suppression signal is a time-varying signal, wherein the stimulation signal is a low- frequency signal and the suppression signal is a high-frequency signal. An amplitude of the stimulation signal may vary with a frequency in the range of 0.1 - 100 Hz, whereas an amplitude of the suppression signal may vary with a frequency in the range of 1 - 10 kHz. According to an embodiment, a method for at least partly denervating an effector tissue of a patient is provided. The method comprises temporarily inhibiting a nerve innervating the effector tissue, determining a response measure indicative of an effector response in the effector tissue, wherein the effector response is at least partly induced by the inhibiting of the nerve, comparing the response measure with a predetermined reference measure, and at least partly denervating the effector tissue based at least in part on the comparison. According to an embodiment, a system for at least partly denervating an effector tissue of a patient is provided, comprising an inhibition device configured to temporarily inhibit a nerve innervating the effector tissue, a sensor configured to generate a sensor signal indicative of an effector response in the effector tissue, the effector response being at least partly induced by the inhibiting of the nerve, and a processing unit configured to determine a response measure based on the sensor signal, the response measure being indicative of the effector response, compare the response measure with a predetermined reference measure, and determine, based on the comparison, whether a desired effector response has been achieved. The system further comprises a denervation device configured to at least partly denervate the effector tissue. In an example, the inhibition device comprises a cooling device configured to cool the nerve to cause a temporary inhibition of the nerve. In an example, the inhibition device is a toxin administration device configured to deliver a neurotoxin to the nerve to cause a temporary inhibition of the nerve. The neurotoxin may in an example comprise botulinum toxin. In an example, the inhibition device may be a vibrational device configured to deliver an inhibition signal to the nerve to cause a temporary inhibition of the nerve. In an example, the inhibition device may be an electric stimulation device configured to deliver an inhibition signal to the nerve to cause a temporary inhibition of the nerve. In some examples, the inhibition signal is a periodic signal including at least one of: a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component. An amplitude of the signal may vary in the range of 1 - 10 kHz. In an example, the inhibition signal may be an electric signal comprising a series of pulses having a negative voltage relative to ground. A positive voltage pulse may follow one or more negative voltage pulses. In an example, the inhibition signal may be generated such that a first inhibition electrode serves as a cathode and a second inhibition electrode serves as an anode, the first and second inhibition electrodes being arranged spaced apart along the nerve. In an example, a suppression signal may be delivered to the nerve to suppress action potentials propagating in the nerve in a direction towards the central nervous system. In an example, the suppression signal may be regulated to suppress the action potentials induced in the nerve in response to the inhibition signal. In an example, the inhibition signal may be delivered at a position between the effector tissue and the position in which the suppression signal is applied to the nerve. In an example, the suppression of the action potentials is delivered to inhibit an undesired response of the nervous system of the patient, the undesired response being generated responsive to the electric inhibition signal. In an example, the electric inhibition signal and the suppression signal may be delivered in sequence, with a delay of the suppression signal timed to generally match a conduction velocity of the electric inhibition signal in the nerve. In an example, a sensor signal, indicative of the effector response, may be received at the control unit which may determine the response measure based on the received sensor signal. In an example, the sensor signal may be indicative of an electric activity in the effector tissue. In an example, the sensor signal may be indicative of a change in electrical impedance in the effector tissue. In some examples, the effector tissue may form part of a renal artery of the patient and the sensor signal may be indicative of a vasodilation or vasoconstriction of the renal artery. In some examples, the effector tissue may form part of a gastrointestinal tract of the patient and the sensor signal may be indicative of a level of motility of the gastrointestinal tract. In an example, the effector tissue may be glandular tissue and the sensor signal be indicative of a level of glandular secretion of the glandular tissue. The glandular tissue may form part of at least one of: a pancreas secreting insulin, a gallbladder secreting bile, and an adrenal gland secreting adrenaline, aldosterone, or cortisol. In an example, the effector tissue may be muscle tissue and wherein the sensor signal be indicative of mechanical movement of the muscle tissue. The sensor signal may be generated by a strain gauge measuring a contraction or relaxation of the muscle tissue. In some examples, the sensor signal may be indicative of a heart rate of the patient, a blood pressure of the patient, or a rate of respiration of the patient. In an example, the at least partly denervating of the effector tissue may comprises ablating the effector tissue. The ablating may comprise at least one of: surgical ablation, radiofrequency ablation, cryoablation, laser ablation, heat ablation, laser ablation, electrocautery, and chemical ablation. According to an embodiment, a system for stimulating an effector tissue of a patient is provided. The system comprises a stimulation device configured to deliver a stimulation signal to at least one of the effector tissue and a nerve innervating the effector tissue of the patient, a source of energy configured to energize the stimulation device, a control unit operably connected to the stimulation device and configured to control an operation of the stimulation device such that the stimulation signal causes at least one of an effector response and inhibition of the effector response in the effector tissue, and a capacitor configured to reduce a current leakage of the system to 1 μA or less, such as 0.1 μA or less. It will be appreciated that the capacitor may be implemented in any of the systems of the above-discussed aspects and examples. In an example, the capacitor may be configured to be connected in series with the body of the patient and at least one of the stimulation device, the source of energy, and the control unit. In an example, the stimulation device may comprise an electrode arrangement configured to be coupled to the effector tissue or the nerve. The capacitor may be configured to be connected in series with the body of the patient and the electrode arrangement. In an example, the electrode arrangement may comprise a first stimulation electrode and a second stimulation electrode for applying the stimulation signal. The capacitor may be configured to be connected in series with the first stimulation electrode and the second stimulation electrode. In an example, the capacitor may be integrated in a circuitry for controlling the operation of the stimulation device. In an example, the system may further comprise a printed circuit board, PCB, supporting the capacitor and at least one of the stimulation device, the source of energy, and the control unit. The PCB may be at least one of a multi-layer PCB, a flexible PCB, and a stretchable PCB. According to an embodiment, a system for stimulating an effector tissue of a patient is provided. The system comprises a stimulation device configured to deliver a stimulation signal to at least one of the effector tissue and a nerve innervating the effector tissue of the patient, a source of energy configured to energize the stimulation device, a control unit operably connected to the stimulation device and configured to control an operation of the stimulation device such that the stimulation signal causes at least one of an effector response and inhibition of the effector response in the effector tissue, and a printed circuit board (PCB), supporting at least one of the stimulation device, the source of energy, and the control unit. The PCB is at least one of a multi-layer PCB, a flexible PCB, a stretchable PCB. It will be appreciated that the PCB may be implemented in any of the systems of the above-discussed aspects and examples. In an example, the PCB may comprise a first multi-layer portion and a second multi-layer portion interconnected by a stretchable portion. In an example, the PCB may comprise a first multi-layer portion and a second multi-layer portion interconnected by a flexible portion. According to an embodiment, a method for affecting a balance between a sympathetic tone and parasympathetic tone of the autonomic nervous system of a patient is provided. The method comprises: delivering, by a first stimulation arrangement, a first stimulation signal to a sympathetic nerve of the patient to increase a level of activity of the sympathetic nerve and move the balance towards a sympathetic dominance, or delivering, by a second stimulation arrangement, a second stimulation signal to the parasympathetic nerve to increase a level of activity of the parasympathetic nerve and move the balance towards a parasympathetic dominance. In an example, each of the sympathetic nerve and the parasympathetic nerve forms part of at least one of: a cardiovascular system, a respiratory system, a gastrointestinal tract, a urinary system, an immune system, a sexual function, and a stress response system. In an example, the first stimulation signal is delivered to the vagus nerve. In an example, the first stimulation signal is delivered to the celiac branch of the vagus nerve. In an example, the first stimulation signal is delivered to the sacral plexus. In an example, at least one of the first stimulation signal and the second stimulation signal is delivered to the cardiac plexus. In an example, at least one of the first stimulation signal and the second stimulation signal is delivered to the pulmonary plexus. In an example, the second stimulation signal is delivered to the celiac plexus. In an example, the second stimulation signal is delivered to the hypogastric plexus. In an example, the first stimulation signal is delivered to the pelvic plexus. In an example, at least one of the first stimulation signal and the second stimulation signal is delivered to the hypothalamus. In an example, at least one of the first stimulation signal and the second stimulation signal is delivered to the brainstem. In an example, at least one of the first stimulation signal and the second stimulation signal is delivered to the midbrain, the pons, or the medulla oblongata. In an exmple, each of the first and second stimulation signals is a periodic signal including at least one of: a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component. In an example, each of the first stimulation signal and the second stimulation signal comprises an amplitude varying with a frequency in the range of 0.1-100 Hz. In an example, at least one of the first and second stimulation signals comprises series of pulses having a negative voltage relative to ground. In an example, the method method comprises generating a positive voltage pulse following one or more negative voltage pulses. In an example, at least one of the first stimulation signal and the second stimulation signal is an electric signal or a vibrational signal. In an example, the method further comprises: receiving a sensor signal indicating an activity in the sympathetic nerve in response to the first stimulation signal, or an activity in the parasympathetic nerve in response to the second stimulation signal; and adjusting an intensity of at least one of the first stimulation signal and the second stimulation signal based at least in part on the sensor signal. In an example, the sensor signal indicates an electric activity in the sympathetic nerve and / or the parasympathetic nerve. In an example, the sensor signal indicates a change in electrical impedance in the sympathetic nerve and / or the parasympathetic nerve. In an example, the method comprisese delivering the first stimulation signal by a first stimulation electrode and a second stimulation electrode arranged spaced apart along the sympathetic nerve. In an example, the method comprises delivering the first stimulation signal such that the first stimulation electrode serves as a cathode and the second stimulation electrode serves as an anode. In an example, the method comprises delivering the second stimulation signal by a third stimulation electrode and a fourth stimulation electrode arranged spaced apart along the parasympathetic nerve. In an example, the method comprises delivering the second stimulation signal such that the third electrode serves as a cathode and the fourth electrodes serves as an anode. In an example, the method comprises: applying a first suppression signal to the sympathetic nerve to suppress action potentials generated by the first stimulation signal and propagating in a direction towards the central nervous system. In an example, the method comprises: regulating the suppression of the action potentials to inhibit an undesired response of the nervous system of the patient, the undesired response being generated responsive to the first stimulation signal. In an example, the method comprises: applying the first stimulation signal and the first suppression signal in sequence, with a delay of the first suppression signal timed to generally match a conduction velocity of the first stimulation signal in the sympathetic nerve. In an example, an amplitude of the first suppression signal varies with frequency in the range of 1-10 kHz. In an example, the method further comprises: applying a second suppression signal to the parasympathetic nerve to suppress action potentials generated by the second stimulation signal and propagating in a the direction towards the central nervous system. In an example, the method comprises: regulating the suppression of the action potentials to inhibit an undesired response of the nervous system of the patient, the undesired response being generated responsive to the second stimulation signal. In an example, the method comprises: applying the second stimulation signal and the second suppression signal in sequence, with a delay of the second suppression signal timed to generally match a conduction velocity of the second stimulation signal in the parasympathetic nerve. In an example, an amplitude of the second suppression signal varies with frequency in the range of 1-10 kHz. According to an embodiment, a system for reducing pain in a patient is provided, comprising: a stimulation device configured to deliver, directly or indirectly, a suppression signal to a nerve of the patient; a control unit configured to control an operation of the stimulation device to suppress or block a propagation of action potentials in an afferent direction of the nerve, thereby reducing the patient’s sensation of pain originating from the action potentials. In an example, the pain is a phantom pain. In an example, the control unit is configured to control the operation of the stimulation device such that the suppression signal is a time-varying signal with a frequency in the range of 1-10 kHz. In an example, the system further comprises a sensor device configured to generate a sensor signal indicating the action potentials propagating in the nerve. In an example, the control unit is configured to receive the sensor signal and to control an operation of the stimulation device based at least in part on the sensor signal. In an example, the stimulation device comprises a suppression electrode configured to be coupled to the nerve to deliver the suppression signal to the nerve, and wherein the sensor device comprises a sensor electrode configured to be arranged cranial to the suppression electrode. In an example, the control unit is configured to increase an intensity of the suppression signal in response to action potentials passing by the suppression electrode in the cranial direction. In an example, the control unit is configured to control the operation of the stimulation device such that the suppression signal is a periodic signal including at least one of: a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component. In an example, the suppression signal comprises a series of pulses having a negative voltage relative to ground. In an example, the control unit is configured to operate the stimulation device to generate a positive voltage pulse following one or more negative voltage pulses. In an example, the stimulation device comprises a first suppression electrode and a second suppression electrode, the first suppression electrode and the second suppression electrode being configured to be spaced apart along the nerve. In an example, the stimulation device is configured to generate the suppression signal such that the first suppression electrode serves as a cathode and the second suppression electrode serves as an anode. In an example, the system further comprises a cuff configured to be at least partially arranged around the nerve and to hold the first suppression electrode and / or the second suppression electrode in place against the nerve. According to an embodiment, a method of creating engorgement of an erectile body of a male person is provided. The method involves using a pre-implanted stimulation device comprising configured to deliver a first stimulation signal to a sympathetic nerve innervating a penile vein of the male person and to deliver a second stimulation signal to a parasympathetic nerve innervating a penile artery of the male person. The method comprising: stimulating, by means of the first stimulation signal, the sympathetic nerve to cause vasoconstriction of the penile vein; stimulating, by means of the second stimulation signal, the parasympathetic nerve to cause vasodilation of the penile artery; wherein the vasodilation of the penile artery increases a blood flow entering the erectile body of the penis and the vasoconstriction of the penile vein reduces a blood flow exiting the erectile body, thereby inducing engorgement of the erectile body. In an example, the method comprises delivering the first stimulation signal to the sympathetic nerve at a position between a level of the T11-L2 vertebrae and the pelvic plexus; and delivering the second stimulation signal to the parasympathetic nerve at a position between a level of sacral spinal cord segments S2-S4 and the pelvic plexus. In an example, each of the first and second stimulation signals is a periodic signal including at least one of: a variable frequency component, a variably duty cycle component, a variable amplitude component, and a variable pause component. In an example, the method comprises: delivering a first inhibition signal to the sympathetic nerve to cause vasodilation of the penile vein; and delivering a second inhibition signal to the parasympathetic nerve to cause vasoconstriction of the penile artery. In an example, the first stimulation signal is a low-frequency signal configured to stimulate the activity of the sympathetic nerve; the second stimulation signal is a low-frequency signal configured to stimulate the activity of the parasympathetic nerve; the first inhibition signal is a high-frequency signal configured to inhibit the activity of the sympathetic nerve; and the second inhibition signal is a high-frequency signal configured to inhibit the activity of the parasympathetic nerve. In an example, the method comprises: varying an amplitude of the low-frequency signal with a frequency in the range of 0.1-100 Hz; and varying an amplitude of the high-frequency signal with a frequency in the range of 1-10 kHz. In an example, at least one of the first and second stimulation signals comprises series of pulses having a negative voltage relative to ground. In an example, a positive voltage pulse follows one or more negative voltage pulses. In an example, at least one of the first stimulation signal and the second stimulation signal is an electric signal or a vibrational signal. In an example, the method further comprises: receiving a sensor signal indicating at least one of vasoconstriction of the penile vein, vasodilation of the penile artery, and engorgement of the erectile body; and adjusting an intensity of at least one of the first and second stimulation signal based at least in part on the sensor signal. In an example, the sensor signal indicates an electric activity in smooth muscle tissue of the penile vein and / or the penile artery. In an example, the sensor signal indicates a change in electrical impedance in smooth muscle tissue of the penile vein and / or the penile artery. In an example, the sensor signal is generated by a strain gauge and wherein the sensor signal indicates an engorgement of the erectile body. In an example, the method comprises determining a response measure based on the sensor signal, the response measure being indicative of said at least one of vasoconstriction of the penile vein, vasodilation of the penile artery, and engorgement of the erectile body. In an example, the method comprises: comparing the response measure with a predetermined reference measure; and in response to the response measure being below the reference measure, increasing an intensity of the first stimulation signal to stimulate the activity in the in the sympathetic nerve and / or increasing an intensity of the second stimulation signal to increase the activity of the parasympathetic nerve, and in response to the response measure exceeding the reference measure, reducing the intensity of the first stimulation signal to inhibit the activity of the sympathetic nerve and / or reducing the intensity of the second stimulation signal to inhibit the activity of the parasympathetic nerve. In an example, the predetermined reference measure is based on a previous measurement on the male person. In an example, the predetermined reference measure is based on previous measurement on other male persons. In an example, the method further comprises applying a first suppression signal to the sympathetic nerve to suppress action potentials generated by the first stimulation signal and propagating in a direction towards the central nervous system. In an example, the method comprises applying the first stimulation signal at a position between the penile vein and a position in which the first suppression signal is applied. In an example, the method comprises regulating the suppression of the action potentials to inhibit an undesired response of the nervous system of the male person, the undesired response being generated responsive to the first stimulation signal. In an example, the method comprises applying the first stimulation signal and the first suppression signal in sequence, with a delay of the first suppression signal timed to generally match a conduction velocity of the first stimulation signal in the sympathetic nerve. In an example, an amplitude of the first suppression signal varies with frequency in the range of 1-10 kHz. In an example, the method further omprises applying a second suppression signal to the parasympathetic nerve to suppress action potentials generated by the second stimulation signal and propagating in the direction towards the central nervous system. In an example, the method comprises applying the second stimulation signal at a position between the penile artery and a position in which the second suppression signal is applied. In an example, the method comprises regulating the suppression of the action potentials to inhibit an undesired response of the nervous system of the male person, the undesired response being generated responsive to the second stimulation signal. In an example, the method comprises applying the second stimulation signal and the second suppression signal in sequence, with a delay of the second suppression signal timed to generally match a conduction velocity of the second stimulation signal in the parasympathetic nerve. In an example, an amplitude of the second suppression signal varies with frequency in the range of 1-10 kHz. In an example, the method comprises delivering the first stimulation signal by means of a first electrode and a second electrode arranged spaced apart along the sympathetic nerve. In an example, the method comprises stimulating the sympathetic nerve by operating the first electrode as a cathode and the second electrode as an anode. In an example, the method comprises delivering the second stimulation signal by means of a third electrode and a fourth electrode arranged space apart along the parasympathetic nerve. In an example, the method comprises stimulating the parasympathetic nerve by operating the third electrode as a cathode and the fourth electrode as an anode. According to an embodiment, a system for treating erectile dysfunction in a male person is provided, comprising: a stimulation device configured to deliver, directly or indirectly: a first stimulation signal to a sympathetic nerve innervating a penile vein of the person; a second stimulation signal to a parasympathetic nerve innervating a penile artery of the person; and a control unit configured to control an operation of the stimulation device such that: the first stimulation signal stimulates an activity of the sympathetic nerve, thereby causing vasoconstriction of the penile vein; and the second stimulation signal stimulates an activity of the parasympathetic nerve, thereby causing vasodilation of the penile artery; wherein the vasodilation of the penile artery increases a blood flow entering an erectile body of the penis and the vasoconstriction of the penile vein reduces a blood flow exiting the erectile body, thereby inducing engorgement of the erectile body. In an example, the system comprises : a first stimulation arrangement configured to deliver the first stimulation signal, the first stimulation arrangement being configured to be coupled to the sympathetic nerve at a position between a level of the T11-L2 vertebrae and the pelvic plexus; and a second stimulation arrangement configured to deliver the second stimulation signal, the second stimulation arrangement being configured to be coupled to the second stimulation signal to the parasympathetic nerve at a position between a level of sacral spinal cord segments S2-S4 and the pelvic plexus. In an example, the control unit is configured to control the operation of the stimulation device such that at least one of the first stimulation signal and the second stimulation signal is a periodic signal including at least one of: a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component. In an example, each of the first stimulation signal and the second stimulation signal comprises an amplitude varying with a frequency in the range In an example, at least one of the first and second stimulation signals comprises series of pulses having a negative voltage relative to ground. In an example, the control unit is configured to operate the stimulation device to generate a positive voltage pulse following one or more negative voltage pulses. In an example, at least one of the first stimulation signal and the second stimulation signal is an electric signal or a vibrational signal. In an example, the system further comprises a sensor device configured to generate a sensor signal indicating at least one of vasoconstriction of the penile vein, vasodilation of the penile artery, and engorgement of the erectile body, wherein the control unit is configured to receive the sensor signal and to control an operation of the stimulation device based at least in part on the sensor signal. In an example, the sensor device comprises a sensor electrode configured to measure an electric activity in smooth muscle tissue of the penile vein and / or the penile artery. In an example, the device comprises a sensor electrode configured to measure a change in electrical impedance in smooth muscle tissue of the penile vein and / or the penile artery. In an example, the sensor electrode is configured to be arranged at the penile vein and / or the penile artery, the sensor further comprises a reference electrode, and the sensor device is configured to generate the sensor signal based on an electrical interaction between the sensor electrode and the reference electrode. In an example, the reference electrode is formed by a housing of the stimulation device or the sensor device. In an example, the sensor signal is generated by a strain gauge and wherein the sensor signal indicates an engorgement of the erectile body. In an example, the control unit is configured to determine a response measure based on the sensor signal, the response measure being indicative of said at least one of vasoconstriction of the penile vein, vasodilation of the penile artery, and engorgement of the erectile body. In an example, the control unit is configured to: compare the response measure with a predetermined reference measure; and in response to the response measure being below the reference measure, increase an intensity of the first stimulation signal to stimulate the activity in the in the sympathetic nerve and / or increase an intensity of the second stimulation signal to increase the activity of the parasympathetic nerve, and in response to the response measure exceeding the reference measure, reduce the intensity of the first stimulation signal to inhibit the activity of the sympathetic nerve and / or reduce the intensity of the second stimulation signal to inhibit the activity of the parasympathetic nerve. In an example, the predetermined reference measure is based on a previous measurement on the person. In an example, the predetermined reference measure is based on previous measurement on other persons. In an example, the stimulation device comprises a first stimulation arrangement configured to deliver the first stimulation signal and a second stimulation arrangement configured to deliver the second stimulation signal. In an example, the first stimulation arrangement comprises a first stimulation electrode and a second stimulation electrode, the first stimulation electrode and the second stimulation electrode are configured to be spaced apart along the sympathetic nerve innervating the penile vein of the person. In an example, the stimulation device is configured to generate the first stimulation signal such that the first stimulation electrode serves as a cathode and the second stimulation electrode serves as an anode. In an example, the system further comprises a cuff configured to be at least partially arranged around the sympathetic nerve and to hold the first stimulation arrangement in place against the sympathetic nerve. In an example, the second stimulation arrangement comprises a third electrode and a fourth electrode, the third electrode and the fourth electrode being configured to be arranged spaced apart along the parasympathetic nerve. In an example, the stimulation device is configured to generate the second stimulation signal such that the third electrode serves as a cathode and the fourth electrodes serves as an anode. In an example, the system further comprises a cuff configured to be at least partially arranged around the parasympathetic nerve and to hold the second stimulation arrangement in place against the parasympathetic nerve. In an example, the system further comprises a suppression device comprising a first suppression arrangement configured to apply a first suppression signal to the sympathetic nerve to suppress action potentials generated by the first stimulation signal and propagating in a direction towards the central nervous system. In an example, the stimulation device is configured to deliver the first stimulation signal to the sympathetic nerve at a position between the penile vein and the first suppression arrangement. In an example, the control unit is configured to regulate the suppression of the action potentials to inhibit an undesired response of the nervous system of the person, the undesired response being generated responsive to the first stimulation signal. In an example, the control unit is configured to apply the first stimulation signal and the first suppression signal in sequence, with a delay of the first suppression signal timed to generally match a conduction velocity of the first stimulation signal in the sympathetic nerve. In an example, the suppression device is configured to vary an amplitude of the first suppression signal with frequency in the range of 1-10 kHz. In an example, the first suppression arrangement comprises a first suppression electrode and a second suppression electrode configured to be spaced apart along the sympathetic nerve. In an example, the first suppression arrangement further comprises a third suppression electrode configured to be arranged spaced apart from the first and second suppression electrodes along the sympathetic nerve such that the second suppression electrode is arranged between the first and third suppression electrodes. In an example, the suppression device is configured to generate the first suppression signal such that the second suppression electrode serves as a cathode and the first and third suppression electrodes serve as anodes. In an example, the system further comprises a suppression device comprising a second suppression arrangement configured to apply a second suppression signal to the parasympathetic nerve to suppress action potentials generated by the second stimulation signal and propagating in a the direction towards the central nervous system. In an example, the stimulation device is configured to deliver the second stimulation signal to the parasympathetic nerve at a position between the penile artery and the second suppression arrangement. In an example, the control unit is configured to regulate the suppression of the action potentials to inhibit an undesired response of the nervous system of the person, the undesired response being generated responsive to the second stimulation signal. In an example, the suppression device is configured to apply the second stimulation signal and the second suppression signal in sequence, with a delay of the second suppression signal timed to generally match of conduction velocity of the second stimulation signal in the parasympathetic nerve. In an example, the suppression device is configured to vary an amplitude of the second suppression signal with frequency in the range of 1-10 kHz. In an example, the second suppression arrangement comprises a first suppression electrode and a second suppression electrode configured to be spaced apart along the parasympathetic nerve. In an example, the first suppression arrangement further comprises a third suppression electrode configured to be arranged spaced apart from the first and second suppression electrodes along the parasympathetic nerve such that the second suppression electrode is arranged between the first and third suppression electrodes. In an example, the suppression device is configured to generate the second suppression signal such that the second suppression electrode serves as a cathode and the first and third suppression electrodes serve as anodes. According to an embodiment, a system for controlling appetite in a patient is provided, comprising: a stimulation device configured to deliver, directly or indirectly a stimulation signal to the vagus nerve; and a control unit configured to control an operation of the stimulation device to affect a propagation of action potentials in the vagus nerve such that the patient’s feeling of satiety or hunger is affected. In an example, the control unit is configured to control the operation of the stimulation device such that the stimulation signal suppresses the propagation of action potentials in a cranial direction, thereby hindering a hunger signal conveyed by the vagus nerve from reaching the patient’s brain. In an example, the control unit is configured to control the operation of the stimulation device such that the stimulation signal is a time-varying signal with an amplitude varying with a frequency in the range of 1-10 kHz. In an example, the control unit is configured to control the operation of the stimulation device such that the stimulation signal generates action potentials propagating in a cranial direction, thereby causing a satiety signal to be conveyed by the vagus nerve to the patient’s brain. In an example, control unit is configured to control the operation of the stimulation device such that the stimulation signal is a time-varying signal with an amplitude varying with a frequency in the range of 0.1-100 Hz. In an example, the control unit is configured to control the operation of the stimulation device such that the stimulation signal affects the propagation of action potentials in the vagus nerve to suppress a stomach peristalsis. In an example, the control unit is configured to control the operation of the stimulation device such that the stimulation signal stimulates an activity of a parasympathetic nerve fiber of the vagus nerve innervating muscle tissue of the stomach wall. In an example, control unit is configured to control the operation of the stimulation device such that the stimulation signal is a time-varying signal with an amplitude varying with a frequency in the range of 0.1-100 Hz. In an example, the control unit is configured to control the operation of the stimulation device such that the stimulation signal suppresses the propagation of action potentials in a sympathetic fiber of the vagus nerve innervating muscle tissue of the stomach wall. In an example, the control unit is configured to control the operation of the stimulation device such that the stimulation signal is a time-varying signal with an amplitude varying with a frequency in the range of 1-10 kHz. In an example, the stimulation device comprises a stimulation arrangement configured to deliver the stimulation signal to the vagus nerve, wherein the stimulation arrangement is configured to be coupled to the vagus nerve at a position caudal to the esophageal hiatus. In an example, the stimulation arrangement is configured to be coupled to an esophageal plexus of the vagus nerve. In an example, the stimulation arrangement is configured to be coupled to an anterior trunk of the vagus nerve. In an example, the stimulation arrangement is configured to be coupled to a gastric branch of the vagus nerve. In an example, the stimulation device comprises a suppression arrangement configured to be coupled to the vagus nerve, wherein the control unit is configured to drive the stimulation device to apply, by means of the suppression arrangement, a suppression signal suppressing action potentials propagating in a direction towards the central nervous system in response to the stimulation device applying the stimulation signal. In an example, the stimulation device comprises a stimulation arrangement configured to deliver the stimulation signal to the vagus nerve, wherein the suppression arrangement is configured to be coupled to the vagus nerve caudal to the stimulation arrangement. In an example, the control unit is configured to regulate the suppression of the action potentials so as to inhibit an undesired response of the nervous system of the patient, the undesired response being generated responsive to the stimulation arrangement applying the stimulation signal. In an example, the control unit is configured to drive the stimulation device such that the stimulation arrangement and the suppression arrangement are actuated in sequence, with a delay of the suppression signal timed to generally match a conduction velocity of the stimulation signal in the vagus nerve. In an example, the control unit is configured to drive the stimulation device to apply the stimulation signal and the suppression signal substantially at the same time. In an example, the control unit is configured to drive the stimulation device such that each f other stimulation signal and the suppression signal is a time-varying signal, wherein the stimulation signal is a low-frequency signal and the suppression signal is a high- frequency signal. In an example, an amplitude of the stimulation signal varies with a frequency in the range 100 Hz and wherein an amplitude of the suppression signal varies with a frequency in the range of 1-10 kHz. In an example, the system further comprises a sensor device configured to generate a sensor signal indicating an effector response in tissue innervated by the vagus nerve and / or the action potentials propagating in the vagus nerve. In an example, the control unit is configured to receive the sensor signal and to control an operation of the stimulation device based at least in part on the sensor signal. In an example, the control unit is configured to determine a response measure based on the sensor signal, the response measure being indicative of the effector response. In an example, the control unit is configured to: compare the response measure with a predetermined reference measure; and control the stimulation device to: increase an intensity of the stimulation signal in response to the response measure being below the reference measure, and reduce the intensity of the stimulation signal in response to the response measure exceeding the reference measure. In an example, the control unit is configured to: increase the intensity of the stimulation signal by increasing at least one of a frequency, current amplitude, and voltage amplitude of the stimulation signal; and reduce the intensity of the stimulation signal by reducing at least one of the frequency, current amplitude, and voltage amplitude of the stimulation signal. In an example, the predetermined reference measure is based on a previous measurement of the effector response in the patient. In an example, the predetermined reference measure is based on previous measurements of effector responses in other patients. In an example, the control unit is configured to monitor the level of effector response over time, and to control the stimulation device based on a change rate in the effector response over time. According to an embodiment, there is provided an implantable vibration device comprising: a vibration generating unit (VGU)configured to cause the implantable vibration device to vibrate, wherein the vibration generating unit comprises at least one piezoelectric material, and a wireless energy receiver (R) configured to receive wireless energy to be used, directly or indirectly, by the vibration generating unit, and a casing enclosing at least the vibration generating unit. In an example, the casing further encloses the wireless energy receiver (R). In an example, the wireless energy receiver is provided outside the casing and coupled to the vibration generating unit through a lead. In an example, the implantable vibration device further comprises a rechargeable energy storage unit provided within the casing, for storing at least part of the received wireless energy. In an example, the implantable vibration device comprises an internal controller. In an example, the internal controller is configured to wirelessly receive vibration control data for controlling the vibration of the implantable vibration device. In an example, the internal controller is configured to receive the vibration control data wirelessly via the wireless energy receiver. In an example, the casing further encloses the internal controller. In an example, the piezoelectric material is a ceramic piezoelectric material. In an example, the piezoelectric material is lead zirconate titanate, PZT. In an example, the piezoelectric material is barium titanate. In an example, the piezoelectric material is lead titanate. In an example, the piezoelectric material is a polymeric piezoelectric material. In an example, the polymeric piezoelectric material is polyvinylidene fluoride, PVDF. In an example, the piezoelectric material is comprised in a piezoelectric motor. In an example, the piezoelectric motor is a piezoelectric inchworm motor. In an example, the piezoelectric motor is a piezoelectric inertial motor. In an example, the piezoelectric motor is a piezoelectric walk-drive motor. In an example, the piezoelectric motor is a linear piezoelectric motor. In an example, the vibration generating unit is attached to the casing, so that vibrations generated by the vibration generating unit can travel to the casing. In an example, the piezoelectric motor is a rotational piezoelectric motor. In an example, the vibration generating unit further comprises an weight configured to be eccentrically rotated by the rotational piezoelectric motor. In an example, the vibration generating unit is configured to cause the implantable vibration device to vibrate at a frequency in the range of 1–150 Hz, such as in the range of 35–150 Hz. In an example, the vibration generating unit is configured to cause the implantable vibration device to vibrate at an amplitude of at least 1 mm. In an example, the implantable vibration device comprises an outer surface and a coating arranged on the outer surface. In an example, the coating comprises at least one layer of a biomaterial. In an example, the biomaterial comprises at least one drug or substance with one or more of the following characteristics: an antithrombotic, an antibacterial and an antiplatelet characteristic. In an example, the biomaterial is fibrin-based. In an example, further comprising a second coating arranged on the first coating. In an example, the second coating is of a different biomaterial than said first coating. In an example, the first coating comprises a layer of perfluorocarbon chemically attached to the surface, and wherein the second coating comprises a liquid perfluorocarbon layer. In an example, the coating comprises a drug encapsulated in a porous material. In an example, the surface comprises a metal. In an example, the metal comprises at least one of the following, titanium, cobalt, nickel, copper, zinc, zirconium, molybdenum, tin or lead. In an example, the surface comprises a micro pattern. In an example, the surface further comprises a layer of a biomaterial coated on the micro pattern. In an example, the vibration generating unit is substantially non-magnetic. In an example, the vibration generating unit is substantially non-metallic. In an example, the piezoelectric motor is a reversable piezoelectric motor. According to an embodiment, a medical system is provided, comprising an external device configured for communication with an implantable medical device when implanted in a patient, wherein the medical device comprises a stimulation device according to any of the above embodiments. Any embodiment, part of embodiment, example, method or part of method may be combined in any applicable way within the terms of the appended claims. Brief description of drawings The inventive concept is now described, by way of example, with reference to the accompanying drawings, in which: Figure 1A shows an example of a system for affecting an effector response in a patient. Figures 1B to 1E show various examples of electrodes and electrode arrangements. Figures 2A and B show diagrams illustrating electric stimulation signals Figure 3A shows an example of a system for affecting an effector response in effector tissue of a patient. Figures 3B to 3F show various examples of electrodes and electrode arrangements. Figures 4A-C are diagrams illustrating signals as applied in the context of the present inventive concept. Figure 5A shows an example of a system comprising a sensor device for generating feedback indicative of an effector response. Figs.5B to 5D show various examples of sensor devices. Figure 6 is a schematic outline of a system according to the inventive concept. Figure 7A shows an example of a multi-layer PCB. Figure 7B shows an example of a stretchable PCB. Figure 8A shows an example of a system comprising an inhibition device and a denervation device. Figures 8B-D show various examples of inhibition and denervation devices. Figure 9 is a schematic illustration of the spinal autonomous nerves. Figure 10A shows an example of a system for delivering vibrations to nerves innervating erectile tissue of a male person. Figures 10B-D are cross sections of erectile tissue. Figure 11 is an illustration of the vagal nerve and its innervation of the stomach. Figure 12 illustrate the autonomous innervation of the gastrointestinal tract. Figures 13A-B show an example of the kidneys of a human patient, and the blood vessels supplying the kidneys with blood. Figure 14 shows an example of the innervation of the renal arteries leading to the kidneys. Figures 15A-B show the mechanisms of vasoconstriction and vasodilation in a blood vessel. Figures 16-20 show various examples of medical devices implanted to electrically or otherwise induce vasodilation in the renal artery. Figures 21A-D are various examples of sensors. Figures 22A-B illustrate an electrical stimulation device and a sensor implanted at the rental artery. Figure 23 show a system implanted at the renal artery. Figures 24A-B schematically show implantable vibration devices according to the present disclosure. Figure 25 shows, schematically, an embodiment of an inchworm motor. Figure 26 illustrates, schematically, an operation cycle of a piezoelectric inchworm motor. Figure 27 shows, schematically, an embodiment of a piezoelectric inertial motor. Figure 28 shows, schematically, an embodiment of a piezoelectric walk-drive motor. Figure 29 illustrates, schematically, an operation cycle of a piezoelectric walk-drive motor. Figures 30A–B illustrate, schematically, implantable vibration devices comprising an eccentric mechanism operated by a motor. Figure 31 shows, schematically, a Traveling Wave Ultrasonic Motors (TWUSM). Figure 32 shows, schematically, an embodiment of a Standing Wave Ultrasonic Motor (SWUSM). Figure 33 shows, schematically, an embodiment of a linear ultrasonic motor. Figure 34 shows, schematically, an embodiment of an implantable vibration device comprising a piezoelectric vibration generating unit. Figures 35A – 35FH show an embodiment and describe various functions of an implantable controller for controlling the implantable medical device. Figure 35G shows an elevated perspective view from the left of a housing unit. Figure 35H shows a plain view from the left of a housing unit. Figure 35I shows an elevated perspective view from the left of a housing unit. Figure 35J shows a plain view from the left of a housing unit. Figure 35K shows a system overview of an external device comprising a housing unit and a display device in wireless communication with an implanted medical device. Figure 35L shows a system having a first and a second remote control. Figure 35LL shows the second remote control comprised in a housing unit. Figure 35M schematically shows a medical implant when implanted in a patient. Figure 35N shows a flow chart for a method for training a medical implant to recognize a voice command, according to some embodiments. Figure 35O shows a flow chart for a method for using voice commands to control a medical implant, according to some embodiments. Figures 35P-T illustrates implantable medical devices and external devices for transferring wireless energy to the implantable medical devices. Figure 35U illustrates an implantable medical device and an external device configured to transmit data using near field magnetic induction. Figure 35V shows a system including a medical implant when implanted in a patient. Detailed description In the following, a detailed description of embodiments of the invention will be given with reference to the accompanying drawings. It will be appreciated that the drawings are for illustration only and are not in any way restricting the scope of the invention as defined by the appended claims. Thus, any references to directions, such as “up” or “down”, are only referring to the directions shown in the figures. It should be noted that the features having the same reference numerals generally may have the same function. A feature in one embodiment could thus be exchanged for a feature from another embodiment having the same reference numeral, unless clearly contradictory. The description of the features having the same reference numerals should thus be seen as complementing each other in describing the fundamental idea of the feature and thereby showing the versatility of the feature. Muscle tissue is generally formed of muscle cells that are joined together in tissue that can be either striated or smooth, depending on the presence or absence, respectively, of organized, regularly repeated arrangements of myofibrillar contractile proteins called myofilaments. Striated muscle tissue is further classified as either skeletal or cardiac muscle tissue. Skeletal muscle tissue is typically subject to conscious control and anchored by tendons to bone. Cardiac muscle tissue is typically found in the heart and not subject to voluntary control. A third type of muscle tissue is the so-called smooth muscle tissue, which is typically neither striated in structure nor under voluntary control. Smooth muscle tissue can be found in the walls of blood vessels and the gastrointestinal tract, for example. The contraction of the muscle tissue may be activated both through the interaction of the nervous system as well as by hormones. The different muscle tissue types may vary in their response to neurotransmitters and endocrine substances depending on muscle type and the exact location of the muscle. A nerve is an enclosed bundle of nerve fibers called axons, which are extensions of individual nerve cells or neurons. The axons are electrically excitable, due to maintenance of voltage gradients across their membranes, and provide a common pathway for the electrochemical nerve impulses called action potentials. An action potential may be understood as an all-or-nothing electrochemical pulse generated by the axon if the voltage across the membrane changes by a large enough amount over a short interval. The action potentials travel from one neuron to another by crossing a synapse, where the message is converted from electrical to chemical and then back to electrical. The distal terminations of an axon are called axon terminals and comprise synaptic vesicles storing neurotransmitters. The axonal terminals are specialized to release the neurotransmitters into an interface or junction between the axon and the muscle cell. The released neurotransmitter binds to a receptor on the cell membrane of the muscle cell for a short period of time before it is dissociated and hydrolyzed by an enzyme located in the synapse. This enzyme quickly reduces the stimulus to the muscle, which allows the degree and timing of muscular contraction to be regulated delicately. The action potential in a normal skeletal muscle cell is similar to the action potential in neurons and is typically about -90 mV. Upon activation, the intrinsic sodium / potassium channel of the cell membrane is opened, causing sodium to rush in and potassium to trickle out. As a result, the cell membrane reverses polarity and its voltage quickly jumps from the resting membrane potential of -90 mV to as high as +75 mV as sodium enters. The muscle action potential lasts roughly 2-4 ms, the absolute refractory period is roughly 1-3 ms, and the conduction velocity along the muscle is roughly 5 m / s. This change in polarity causes in turn the muscle cell to contract. The contraction and relaxation of smooth muscle cells is typically influenced by multiple inputs such as spontaneous electrical activity, neural and hormonal inputs, local changes in chemical composition, and stretch. This in contrast to the contractile activity of skeletal and cardiac muscle cells, which may rely on a single neural input. Some types of smooth muscle cells are able to generate their own action potentials spontaneously, which usually occur following a pacemaker potential or a slow wave potential. However, the rate and strength of the contractions can be modulated by external input from the autonomic nervous system. Autonomic neurons may comprise a series of axon-like swellings, called varicosities, forming motor units through the smooth muscle tissue. The varicosities comprise vesicles with neurotransmitters for transmitting the signal to the muscle cell. The autonomic neurons may for example trigger a muscular response in the wall of the renal artery, leading to a contraction or relaxation affecting a flow resistance in the renal artery. Sympathetic stimulation (norepinephrine) has been observed to constrict some blood vessels and dilate others, depending on whether the target cells (i.e., the smooth muscle cells) has alpha- or beta-adrenergic receptors. The sympathetic nervous system can also constrict or dilate vessels just by changing firing frequency of the action potentials. An increased firing frequency may cause the smooth muscle to contract and constrict the vessel, whereas a reduced firing frequency may cause the smooth muscle cells to relax, allowing blood pressure to dilate the vessel. The muscle cells described above, i.e., the cardiac, skeletal and smooth muscle cells are known to react to external stimuli, such as electrical stimuli applied by electrodes. A distinction can be made between stimulation transmitted by a nerve and direct electrical stimulation of the muscle tissue. In case of stimulation via a nerve, an electrical signal may be provided to the nerve at a location distant from the actual muscle tissue, or at the muscle tissue, depending on the accessibility and extension of the nerve in the body. The stimulation devices as well as the signal damping devices described in the present disclosure may employ both a direct stimulation of the muscle tissue and stimulation transmitted via a nerve to affect the vasomotor tone. In case of direct stimulation of the muscle tissue, the electrical signal may be provided to the muscle cells by an electrode arranged in direct or close contact with the cells of the renal artery 20. However, other tissue such as fibrous tissue and nerves may of course be present at the interface between the electrode and the muscle tissue, which may result in the other tissue being subject to the electrical stimulation as well. In the context of the present application, the electrical stimulation discussed in connection with the various aspects and embodiments may be provided to the tissue in direct or indirect contact with the implantable medical device. Preferably, the electrical stimulation is provided by one or several electrode elements arranged at the interface or contact surface between the implantable constriction device and the tissue. Thus, the electrical stimulation for exercising the tissue may, in terms of the present disclosure, be considered as a direct stimulation of the tissue. Particularly when contrasted to stimulation transmitted over a distance by a nerve, which may be referred to as an indirect stimulation or nerve stimulation. A control unit or controller is to be understood as any implantable unit capable of controlling the operation of an electrically operated device, such as a stimulation device or a signal damping device. A controller could include an electrical power source or another operation device for operating the stimulation device and the signal damping device. A control unit may also be understood as an element comprising circuitry configured to carry out various functions, such as data storage and processing, and signal generation. The control unit may be configured to transmit the control instructions to the stimulation device over a wired channel or a wireless channel. Further, the control unit may comprise an external part configured to be arranged outside the body of the patient and an internal part configured to be implanted in the patient. The internal and external parts may be configured to communicate wirelessly with each other, for example by means of radiofrequency signals or inductive signals. A control signal is to be understood as any signal capable of carrying information and / or electric power such that for instance the stimulation device can be directly or indirectly controlled. An implantable operation device, sometimes also referred to as a controller, may further be understood as any device or system capable of operating an active implant. An operation device or controller could for example be an actuator such as a hydraulic actuator including for instance a hydraulic pump or a hydraulic cylinder, or a mechanical actuator, such as a mechanical element actuating an implant by pressing or pulling directly or indirectly on the implant, or an electromechanical actuator such as an electrical motor or solenoid directly or indirectly pressing or pulling on the implant. The operation device may comprise a control unit as described above, and / or circuitry configured to carry out such functions. The sympathetic nervous system (SNS) and the parasympathetic nervous system (PNS) form part of the autonomous nervous system (ANS) of the body. The SNS and the PNS control involuntary bodily functions such as, for example, heart rate, blood pressure, digestion, breathing rate, pupil size, blood flow to the muscles, and sexual responses. The SNS is commonly described as the “fight or flight” system, preparing the body for stress or danger, whereas the PNS is commonly referred to as the “rest and digest” system, promoting relaxation, energy storage, and other non-emergency functions. Activation of the SNS may result in increased heart rate, dilated airways, inhibited digestion, dilated pupils, and redirection of blood to muscles. Activation of the PNS may result in decreased heart rate, stimulated digestion, contracted pupils, and relaxation of muscles. For the SNS, the preganglionic neurons generally originate in the thoracic and lumbar regions of the spinal cord, whereas for the PNS the preganglionic neurons generally originate in the brainstem and the sacral region of the spinal cord. The SNS and the PNS may have complementary functions on the same effector tissue, such as an organ or a muscle. For example, the SNS may accelerate the heart rate, while the PNS may slow it down. Both the SNS and the PNS are typically active to some extent all the time, but their relative activities may change depending on the situation. This dynamic balance between the SNS and the PNS is commonly referred to as the “autonomic tone”. The autonomic tone hence implies there is an ongoing, background level of activity in the SNS and PNS. The body may adjust this balance as needed, ramping up sympathetic or parasympathetic activity in response to specific situations. The tone may also capture the systems’ readiness to respond to stimuli. A certain “tone” or baseline activity level may ensure that the system can quickly ramp up or down its activity to adapt to different situations. Therefore, it may be of interest to adjust or affect this tone for therapeutic purposes, for example to affect the general level of stress in the body. Adjusting the level of activity in the SNS and / or the PNS may, for example, be employed to treat a variety of conditions. For example, increasing the PNS activity and / or decreasing the SNS activity can help treating conditions such as anxiety, hypertension, and irritable bowel syndrome (IBS). On the other hand, increasing SNS activity and / or decreasing PNS activity can help treating conditions such as depression, chronic fatigue syndrome, and postural orthostatic tachycardia syndrome (PoTS). In some instances, both systems work together to perform a function. For example, during sexual arousal and ejaculation, both systems are involved in different phases. During sexual arousal, the PNS may cause the arteries in the erectile tissue to dilate to increase the blood flow, whereas the SNS may cause the veins to contract to reduce the blood flow leaving the erectile tissue. The SNS and the PNS are also coopering during urination, wherein the PNS may cause the sphincters to relax and the SNS the bladder to contract. Adjusting or controlling the cooperation between the SNS and PNS may thus be employed to treat impotence and incontinence. The SNS and the PSNS may generally be considered to work together in a dynamic balance between arousal / activation / contraction and relaxation / inhibition / relaxation in the effector tissue innervated by the SNS and the PNS. Hence, the sympathetic activity and the parasympathetic activity may affect the response in the effector tissue, which typically may be a somatic effector tissue or an autonomic effector tissue. Examples of somatic effector tissue include muscular tissue, such as skeletal muscles, whereas examples of autonomic effector tissue include smooth muscle tissue, cardiac muscle tissue, and glandular or epithelial tissue (commonly involved in the production and secretion of various substances such as hormones, enzymes, and sweat). By stimulating a sympathetic nerve and / or a parasympathetic nerve innervating the effector tissue, the effector response may be controlled or affected accordingly. In case of muscular tissue, the effector response may be a contraction or relaxation of the tissue. In case the effector tissue being glandular tissue, the effector response may be an increased or reduced production or secretion of, for example, a hormone or an enzyme. In some examples, the stimulation of the sympathetic nerve and / or parasympathetic nerve may be employed to adjust the autonomic tone discussed above. Generally, ‘effector tissue’ refers to tissues in the body that produce a response or perform work (‘effector response’) when activated by nerve signals. Effectors may essentially be understood as the ‘end targets’ in the signalling pathways of the nervous system. As mentioned above, they may be categorized as muscles (skeletal muscles, smooth muscle) and glands (endocrine glands and exocrine glands). They may furthermore be categorized based on their relationship with the nervous system. The somatic effectors are mostly skeletal muscles controlled by the somatic nervous system, responsible for voluntary actions, whereas the autonomic effectors typically are controlled by the autonomic nervous system and include smooth muscle tissue, cardiac muscle, and glands. These effectors are generally not under voluntary control. It is to be noted that the various aspects of stimulation discussed in the present disclosure may be applied to any type of effector tissue, including somatic effectors as well as autonomic effectors. An exemplary system for affecting an effector response in a patient will now be discussed with reference to Fig.1A to Fig.1E. Fig. 1A is a schematic illustration of a particular example of the system and its interaction with the body of the patient P, and more particularly with an effector tissue 230 innervated by a sympathetic nerve 231 and a parasympathetic nerve 232. As indicated, the sympathetic nerve 231 and the parasympathetic nerve 232 may extend between the effector tissue 230 and the central nervous system (CNS) 233. The sympathetic nerve 231 may, for example, originate from the thoracic or lumbar regions of the spinal cord, whereas the parasympathetic nerve may originate in the brainstem or the sacral region of the spinal cord. In the present example, the origin of the illustrated nerves 231, 232 is represented by item 233. It will be appreciated that the effector tissue 230 and the CNS 233 are merely schematically indicated and that the technology described in the following may be applied to various types of nerves and effector tissues, located in various positions and parts of the body P. In some examples, the sympathetic nerve 231 and the parasympathetic nerve 232 may innervate the same effector tissue 230, which thus may be considered to have a dual autonomous nervous system (ANS) innervation. This means that the effector tissue 230 may receive competing inputs from the sympathetic and the parasympathetic divisions of the ANS. In other examples, the sympathetic nerve 231 may innervate a first effector tissue and the parasympathetic nerve 232 may innervate a second effector tissue, the second effector tissue being different from the first effector tissue 230. In other words, the sympathetic nerve 231 and the parasympathetic nerve 232 may innervate different organs, muscles, or part of a muscle. Both these examples, i.e., in which the sympathetic and parasympathetic nerves 231, 232 innervate the same or different tissue, are represented by item 230. As illustrated, the system comprises a stimulation device configured to deliver, directly or indirectly, a first simulation signal to the sympathetic nerve 231 innervating the first effector tissue 230 and a second stimulation signal to the parasympathetic nerve 232 innervating the second effector tissue 230. The effector tissue 230 may hence be the same effector tissue, forming part of the same muscle or organ, or different effector tissues 230, forming part of different muscles or organs. The system further comprises a control unit or controller 240, configured to control an operation of the stimulation device such that the first stimulation signal stimulates an activity of the sympathetic nerve 231 and the second stimulation signal inhibits an activity of the parasympathetic nerve 232 or such that the first stimulation signal inhibits an activity of the sympathetic nerve 231 and the second stimulation signal stimulates an activity of the parasympathetic nerve 232. Hence, each of the first and second stimulation signals may result either in an activation or an inhibition, depending on the characteristics of the stimulation signal. A signal that results in an activation of the nerve (and / or the effector tissue) may be referred to as an activation signal, whereas a signal that results in an inhibition of the nerve (and / or the effector tissue) may be referred to as an inhibition signal. “Activation of a nerve” is generally to be understood as the generation of a nerve signal, i.e., action potentials travelling in the nerve, whereas “inhibition of a nerve” is generally to be understood as blocking or hindering any nerve signals from propagating through the nerve. Inhibition may also be referred to as a suppression or blocking of the nerve and / or its signals. It should be noted that the blocking may not always be complete; on the contrary, there may still be some activity in the nerve. However, it is preferable to suppress the nerve signal to a degree that results in no or a negligible response in the effector tissue 230. The nervous response, or effector response, may typically be determined by, inter alia, a frequency content of the signal. The signal may be a periodic signal, including at least one of: a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component. Generally, a low-frequency stimulation may be more likely to result in inhibition, whereas high-frequency stimulation tends to excite neural pathways and effector tissue. Further, higher voltages and currents may more often lead to activation as compared to lower voltages and currents. The response to a stimulation signal may however vary based on other factors, such as location and target tissue. It may therefore be beneficial to measure the effect of the stimulation to determine whether the treatment has an intended effect or not and to provide feedback that can be used to adjust the characteristics of the stimulation signal. For example, the measured effect may be used as feedback in a closed loop control of the stimulation device. This will be discussed in further detail later in the present disclosure. The activation signal and the inhibition signal may cooperate to achieve a certain response. For example, the activation and inhibition signals may be applied to an antagonistic muscle pair, where the activation signal may be applied to the agonist to cause it to contract and the inhibition signal may be applied to the antagonist muscle to cause it to relax. Hence, this is an example of the effector tissue 230 forming part of different organs, such as the agonist and the antagonist of an antagonistic muscle pair. In other examples, the activation and inhibition signals may be applied in sequence to the same effector tissue 230, such that an activation (such as a contraction) triggered by the activation signal is followed by an inhibition (such as a relaxation) triggered by the inhibition signal, or vice versa. It is also possible to apply several stimulation signals and / or inhibition signals to several different effector tissues. A first stimulation signal may, for example, be applied to a first effector tissue (such as a first muscle of an antagonistic pair) and a second stimulation signal may be applied to a second effector tissue (such as the other muscle of the antagonistic pair). By applying the first and second stimulation signals in sequence, an improved control and stabilization of body movement may be achieved. The present system can be employed to treat or at least reduce or alleviate muscle spasms, which may be understood as sudden, involuntary contractions of one or more muscles. By applying an inhibition signal to the nerve innervating the muscle that is contracting during the spasm, or by applying the inhibition signal directly to that muscle, the muscle may be caused to relax. Alternatively, or additionally, the activation signal may be applied to a nerve innervating a muscle counteracting the spasming muscle. As the counteracting muscle responds to the activation signal by contracting, it may help balancing or counteracting the spasming muscle. This approach may be particularly useful for addressing symptoms of, for example, a herniated disc, sciatica, spinal stenosis, as well as neurological disorders such as multiple sclerosis, Parkinson’s disease, dystonia, and cerebral palsy. A stimulation signal may have different characteristics, depending on the desired effector response to be achieved. As already mentioned, these characteristics may relate to amplitude, frequency, waveform, polarity, and duty cycle. The duty cycle may be understood as the ratio of the time that the signal is ‘on’, i.e., active, to the total time of one cycle (period). For a pulsed signal, this would correspond to the ratio of the pulse length to the length of a cycle. The duty cycle is usually expressed as a percentage or a fraction. For example, a 50% duty cycle may be understood as the signal being ‘on’ for half of the cycle and ‘off’ for the other half. The duty cycle of an electric stimulation signal can influence the energy delivered to the tissue (or at least the energy to which the tissue is exposed). A higher duty cycle means that the tissue may be exposed to more electric charges and energy, which can increase the stimulation effect, whereas a lower duty cycle means that the tissue may be exposed to less electric charge and energy. A lower duty cycle may mean that the tissue has more time to recover and adapt to the stimulation, which can reduce the risk of tissue damage or fatigue. Different types of tissues may require different duty cycles for optimal stimulation. Electric stimulation signals with low duty cycles (less than 10%) have been shown to promote cell regeneration, proliferation, and growth, whereas electric signals with high duty cycles (more than 50%) have been shown to inhibit cell growth. Generally, duty cycles above 10% may result in a stronger and faster contraction of muscle cells, while duty cycles below 10% may result in a weaker and slower contraction of muscle cells. Accordingly, the pause component of a stimulation signal, describing the time interval between two consecutive pulses or two consecutive pulse trains, can affect the stimulation of tissue in several ways. Increasing the pause component may facilitate recovery from the previous stimulation and reduce the risk of overstimulation or fatigue. A longer pause component can reduce the risk of tissue damage or adaptation, while a shorter pause component can increase the stimulation effect. Furthermore, the pause component may influence the net charge delivered to the tissue and the electrochemical reactions at the electrode–tissue interface. A longer pause component can allow the charge to dissipate and the pH to normalize, while a shorter pause component can cause charge accumulation and pH changes. The pause component may in some examples range from 0.1 - 10 seconds, such as 0.5 - 2 seconds, depending on the tissue type. In an example, a nerve, such as the sympathetic nerve 231 or the parasympathetic nerve 232, may be activated or stimulated by an activation signal comprising a frequency in the range of 0.1 - 100 Hz, such as 1 - 50 Hz. Such a signal may be referred to as a low- frequency signal. The activation signal may comprise a voltage in the range of 1 - 15 V, such as about 10 V and a current in the range of 1 - 50 mA, such as 2 - 4 mA, depending on the target tissue. Applying such a signal to a sympathetic nerve 231 may typically result in an activation of the effector tissue 230, such as a contraction of muscle tissue or an increased secretion of a gland, whereas applying the signal to a parasympathetic nerve 232 may typically result in an inactivation of the effector tissue 230. An inactivation may typically include relaxation of a muscle or a reduced secretion of a gland. Applying such a signal directly to the effector tissue 230 may result in a similar response as applying it to the nerve. To inhibit or inactivate the nerve, an inhibition signal comprising a frequency in the range of 1 - 10 kHz, such a 2 - 5 kHz, can be used. Similar to the activation signal, the voltage can be in the range of 1 - 15 V and the current in the range of 1 - 50 mA. Applying such as signal to a nerve 231, 232 may result in the nerve signals being blocked or at least heavily reduced. As an effect, the effector tissue 230 can be considered more or less cut off from the signals delivered by that nerve from the CNS 233. The control unit 240 may be configured to control the operation of the stimulation device to provide a low-frequency signal for stimulating the activity of the sympathetic nerve 231 and a high-frequency signal for inhibiting the activity of the parasympathetic nerve 232. This may shift the balance between the SNS and PNS activity towards the SNS activity, which may result in a muscle contraction (in case of the effector tissue being a muscle tissue) or increased secretion of a gland (in case of the effector tissue being a glandular tissue). The control unit 240 may as well be configured to control the operation of the stimulation device to provide a high-frequency signal for inhibiting the activity of the sympathetic nerve 231 and a low-frequency signal for stimulating the activity of the parasympathetic nerve 232. This may shift the balance between the SNS and PNS activity towards the PNS activity, which may result in a muscle relaxation (in case of the effector tissue being a muscle tissue) or reduced secretion of a gland (in case of the effector tissue being a glandular tissue). The activation signal and the inhibition signal may be applied to the respective nerves 231, 232 concurrently, simultaneously, or separately, i.e., one at a time. The stimulation device may comprise circuitry and a power source for generating the stimulation signals, which, for example, may be electrical signals or mechanical vibration signals. The circuitry and, optionally, the power source may be arranged within a housing which may be implantable in the body of the patient. Electrical leads may be provided to connect the circuitry to a signal generating means 210, 220 arranged at the respective nerves 231, 232. In case of an electric stimulation signal, the signal generating means 210, 220 may comprise a respective electrode arrangement. In case of a mechanical vibration signal the signal generating means 210, 220 may comprise a respective vibrator, such as a piezoelectric vibrator comprising one or more piezoelectric elements. The vibrations may be generated by the direct movement of the piezoelectric element, or by other mechanical elements actuated by the piezoelectric element. In an example, the vibrations may be generated by an eccentric weight that are brought to rotate by a piezoelectric actuator, such as a rotational motor. At least parts of the stimulation device, such as a housing and / or energy source, may be implanted in fat tissue of the patient, be anchored to bone tissue, or implanted subcutaneously. The control unit 240 may be integrated with the stimulation device, such as arranged within the same housing as the electric circuitry, or the energy source mentioned above. In other examples, the control unit 240 may be arranged separately or remotely, i.e., at a different physical location than the stimulation device. In the latter case, the control unit 240 may be communicatively coupled to the stimulation device by means of a wired or wireless connection. The control unit 240 may hence be arranged within the patient’s body or externally, i.e., outside the body of the patient P. The signal generating means may comprise a first electrode arrangement 210 configured to be coupled to the sympathetic nerve 231 to deliver the first stimulation signal (such as an activation signal or an inhibition signal) and a second electrode arrangement 220 configured to be coupled to the parasympathetic nerve 220 to deliver the second stimulation signal (such as an inhibition signal or an activation signal). Fig.1B to Fig.1E show examples of electrode arrangements which may be implemented in any of the stimulation devices 40 discussed in the present disclosure. Fig.1B is an example of a bipolar electrode arrangement comprising a first and a second electrode element E1, E2, having a plurality of contact portions 122a which can be arranged to abut the sympathetic nerve 231 or the parasympathetic nerve 232 or touch the effector tissue 230. The electrode arrangement may be operated as a bipolar electrode arrangement by connecting the first and second electrode elements E1, E2 to different electrical potentials. Thus, the first electrode element E1 can be operated as an anode and the second electrode element E2 can be operated as a cathode. The electrode elements E1, E2 may be attached directly to a support structure 126, such as a patch, or a cuff 215 as shown in Fig.1E. The electrode arrangement may comprise one or several contact pads or contacting portions 122a, for increasing the contact surface between the electrode and the tissue when implanted. During operation, the stimulation signal may be delivered to the tissue, i.e., the nerve or the effector tissue, by means of the first and second electrode elements E1, E2 to activate or inhibit action potentials in the nerve or activate the effector tissue 230 directly. Fig.1C is another example of an electrode arrangement of an electrical stimulation device as discussed above. In the present example, the electrode arrangement may be operated as a unipolar electrode element or as a bipolar electrode arrangement. The electrode arrangement comprises a first electrode element E1 and a second electrode element E2 which may be formed of a wire or electrical lead arranged in a flat, coiled structure for increasing the contact surface between the electrode elements E1, E2 and the nerve tissue. The electrode elements E1, E2 may be arranged on a flexible and / or stretchable support or patch 216, allowing it to conform to the shape of the tissue to which it is attached and move with any movement of the same. The coiled configuration allows for a certain mechanical flexibility of the electrode elements E1, E2 such that they can move with any movement or deformation of the support 215. Fig.1D illustrates the end portion of a needle-shaped or pin-shaped electrode element E1, E2, wherein the active portion of the electrode element E1, E2 is provided as a bare electrode surface 123 at the end of the electrode element E1, E2. Thus, when implanted at or in the tissue, the active bare electrode surface 123 of the electrode element E1, E2 may form a metal–tissue interface with the tissue. The tip of the bare electrode surface 123 of the electrode element E1, E2 may be inserted into the nerve tissue 231, 232 or arranged to abut an outer surface of the nerve 231, 232. The present example may form a unipolar electrode and may require another electrode, such as a ground electrode, to be arranged elsewhere on the patient’s body to form a closed electric circuit. The completing electrode may, for instance, be formed by a housing of the stimulation device. Figure 1E shows a similar electrode element E1, E2 as the one in figure 1D, with the difference that the present electrode element E1, E2 comprises an active tip portion that is covered by a dielectric material 123’ to protect the electrode material from deterioration during long-term implantation and to facilitate capacitive current transfer to the tissue. The dielectric material 123’ may for instance be electrochemically deposited tantalum oxide, which allow the electrical charge to pass through the interface but reduces the risk for electrode corrosion, gas formation and metabolite reactions. It will be appreciated that both faradaic and capacitive mechanisms may be present at the same time, irrespectively of the type of electrode used. Thus, capacitive charge transfer may be present also for a bare electrode forming a metal–tissue interface, and faradaic charge transfer may be present also for a coated electrode forming a dielectric–tissue interface. It has been found that the faradaic portion of the current delivered to the muscle tissue can be reduced or even eliminated by reducing the duration of the pulses of the electric signal. Reducing the pulse duration has turned out to be an efficient way of increasing the portion of the signal which can be passed through the interface as a capacitive current, rather than by a faradaic current. As a result, shorter pulses may produce less electrode and tissue damage. The capacitive portion of the current may further be increased, relative to the faradaic portion, by reducing the amplitude of the current pulses of the electrical signal. Reducing the amplitude may reduce or suppress the chemical reactions at the interface between the electrode and the tissue, thereby reducing potential damage that may be caused by compounds and ions generated by such reactions. In one example, the electrical stimulation may be controlled in such a manner that a positive pulse of the electrical signal is followed by a negative pulse (or, put differently, a pulse of a first polarity being followed by a pulse of a second, reversed polarity), preferably of the same amplitude and / or duration. Advantageously, the subsequent negative (or reversed) pulse may be used to reverse or at least moderate chemical reactions or changes taking place in the interface in response to the first, positive pulse. By generating a reversed pulse, the risk of deterioration of the electrode and / or the tissue at the interface between the electrode and the muscle tissue may be reduced. In the following, the interaction between an implanted electrode element and tissue of the body will be discussed. This discussion may be applied both to stimulation for inducing an effector response, such as vasodilation, inhibition or blocking of signals, as well as sensing and electrical stimulation for exercising the tissue to reduce effects of deterioration caused by presence of a long term implanted medical device. It has been observed that the interaction between an implanted electrode element and tissue of the body is to a large extent determined by the properties at the junction between the tissue and the electrode element. The active electrically conducting surface of the electrode element (in the following referred to as “metal”, even though other materials is equally conceivable) can either be uncoated resulting in a metal–tissue interface (such as disclosed in figure 1D), or insulated with some type of dielectric material (such as disclosed in figure 1E). The uncoated metal surface of the electrode element may also be referred to as a bare electrode. The interface between the electrode element and the tissue may influence the behavior of the electrode element, since the electrical interaction with the tissue is transmitted via this interface. In the biological medium surrounding the electrode element, such as the actual tissue and any electrolyte that may be present in the junction, the current is carried by charged ions, while in the material of the electrode element the current is carried by electrons. Thus, in order for a continuous current to flow, there needs to be some type of mechanism to transfer charge between these two carriers. In some examples, the electrode element may be a bare electrode wherein the metal may be exposed to the surrounding biological medium when implanted in, or at the muscle tissue that is to be stimulated. In this case there may be a charge transfer at a metal–electrolyte interface between the electrode element and the tissue. Due to the natural strive for thermodynamic equilibrium between the metal and the electrolyte, a voltage may be established across the interface which in turn may cause an attraction and ordering of ions from the electrolyte. This layer of charged ions at the metal surface may be referred to as a “double layer” and may physically account for some of the electrode capacitance. Hence, both capacitive faradaic processes may take place at the electrode element. In a faradaic process, a transfer of charged particles across the metal–electrolyte interface may be considered as the predominant current transfer mechanism. Thus, in a faradaic process, after applying a constant current, the electrode charge, voltage and composition tend to go to constant values. Instead, in a capacitive (non-faradaic) process charge is progressively stored at the metal surface and the current transfer is generally limited to the amount which can be passed by charging the interface. In some examples, the electrode element may comprise a bare electrode portion, i.e., an electrode having an uncoated surface portion facing the tissue such that a conductor–tissue interface is provided between the electrode element and the tissue when the electrode element is implanted. This allows for the electric signal to be transmitted to the tissue by means of a predominantly faradaic charge transfer process. A bare electrode may be advantageous from a power consumption perspective, since a faradaic process tend to be more efficient than a capacitive charge transfer process. Hence, a bare electrode may be used to increase the current transferred to the tissue for a given power consumption. In some examples, the electrode element may comprise a portion that is at least partly covered by a dielectric material so as to form a dielectric-tissue interface with the muscle tissue when the electrode is implanted. This type of electrode element allows for a predominantly capacitive, or non-faradaic, transfer of the electric signal to the muscle tissue. This may be advantageous over the predominantly faradaic process associated with bare electrodes, since faradaic charge transfer may be associated with several problems. Example of problems associated with faradaic charge transfer include undesirable chemical reactions such as metal oxidation, electrolysis of water, oxidation of saline, and oxidation of organics. Electrolysis of water may be damaging since it produces gases. Oxidation of saline can produce many different compounds, some of which are toxic. Oxidation of the metal may release metal ions and salts into the tissue which may be dangerous. Finally, oxidation of organics in a situation with an electrode element directly stimulating tissue may generate chemical products that are toxic. These problems may be alleviated if the charge transfer by faradaic mechanisms is reduced, which may be achieved by using an electrode at least partly covered by a dielectric material. Preferably, the dielectric material is chosen to have as high capacitance as possible, restricting the currents flowing through the interface to a predominantly capacitive nature. Several types of electrode elements can be combined with the present disclosure. The electrode element can for example be a plate electrode as indicated in figure 1B, comprising a plate-shaped active part forming the interface with the tissue. In other examples, the electrode may be a wire electrode as indicated in figure 1C, formed of a conducting wire that can be brought in electrical contact with the tissue. Further examples may include needle- or pin-shaped electrodes as indicated in figure 1D and E, having a point at the end which can be attached to or inserted in the muscle tissue. The electrodes may for example be encased in epoxy for electrical isolation and protection and comprise gold wires or contact pads for contacting the muscle tissue. Preferably, the electrode may be arranged to transmit the electrical signal to the portions of the tissue that is affected, or risks to be affected, by mechanical forces exerted by the medical implant. Thus, the electrode element may be considered to be arranged between the implanted device and the tissue against which the device is arranged to rest when implanted. During operation of the medical device, or the electrode arrangement, the electric signal may cause the muscle cells to contract and relax repeatedly. This action of the cells may be referred to as exercise and may have a positive impact in terms of preventing deterioration and damage of the tissue. Further, the exercise may help increasing tolerance of the tissue for pressure and mechanical forces generated by the medical implant. The contraction and relaxation induced for exercising purposes may thus be less than the effector response induced for the purpose of affecting bodily functions or treating symptoms. Alternatively, or additionally the exercise may involve contraction and relaxation at a relatively high frequency, hindering the blood vessel to contract to a degree that affects the vascular resistance in the vessel before it is relaxed again. The electrical signal for exercising the tissue may be generated by a controller, such as the control unit 150 discussed above in connection with figure 11. The controller 150 may be configured to control the electrical stimulation such that the tissue is stimulated by a series of electrical pulses. The pulses may comprise a pulse of a first polarity followed by a pulse of a second, reversed polarity, and the pulsed electrical stimulation signal generated comprises a pulse frequency of 0.01-150 Hz. In an example, the electrical stimulation signal comprises a pulse duration of 0.01-100 ms and a pulse amplitude of 1-15 mA. Example characteristics of electric signals for exercising the tissue is discussed below with reference to figures 2A and B. The controller may be configured to receive input from a wireless remote control, directly or via a receiver of the implantable controller, for controlling the stimulation or for programming a stimulation routine for exercising the muscle tissue to improve the conditions for long term implantation of the implantable medical device. The programming of a stimulation routine could for example be the programming of the frequency of the stimulation, or the current and / or voltage of the stimulation. It will be appreciated that both faradaic and capacitive mechanisms may be present at the same time, irrespectively of the type of electrode used and the type of stimulation provided (i.e., for the purpose of vasoconstriction / vasodilation, signal damping, or for the purpose of exercising the tissue). Thus, capacitive charge transfer may be present also for a bare electrode forming a metal–tissue interface, and faradaic charge transfer may be present also for a coated electrode forming a dielectric–tissue interface. It has been found that the faradaic portion of the current delivered to the muscle tissue can be reduced or even eliminated by reducing the duration of the pulses of the electric signal. Reducing the pulse duration has turned out to be an efficient way of increasing the portion of the signal which can be passed through the interface as a capacitive current, rather than by a faradaic current. As a result, shorter pulses may produce less electrode and tissue damage. The capacitive portion of the current may further be increased, relative to the faradaic portion, by reducing the amplitude of the current pulses of the electrical signal. Reducing the current may reduce or suppress the chemical reactions at the interface between the electrode and the tissue, thereby reducing potential damage that may be caused by compounds and ions generated by such reactions. In one example, the electrical stimulation may be controlled in such a manner that a positive pulse of the electrical signal is followed by a negative pulse (or, put differently, a pulse of a first polarity being followed by a pulse of a second, reversed polarity), preferably of the same amplitude and / or duration. Advantageously, the subsequent negative (or reversed) pulse may be used to reverse or at least moderate chemical reactions or changes taking place in the interface in response to the first, positive pulse. By generating a reversed pulse, the risk of deterioration of the electrode and / or the tissue at the interface between the electrode and the muscle tissue may be reduced. Fig.1F shows an electrode arrangement 210, 220 comprising a cuff 215 for attachment around the nerve 231, 232. The cuff 215 forms a support structure for the electrode element(s) E1, E2 and allows them to touch the outer surface of the nerve 231, 232. The cuff 215 may be configured to surround or enclose a circumference of the nerve 231, 232 at least partly and may comprise an opening or slit allowing the cuff 215 to be fitted around the nerve 231, 232. One or more of the first and second electrode arrangements 210, 220 may comprise one or more of the electrode elements E1, E2 described above. The electrode elements E1, E2, which may also be referred to as stimulation electrodes, may be spaced apart along the sympathetic nerve 231 and / or the parasympathetic nerve 232. This allows the stimulation device to generate the stimulation signal(s) such that a first one of the stimulation electrodes E1, E2 serves as a cathode and a second one of the stimulation electrodes E1, E2 serves as an anode. It will be appreciated that further electrodes (not shown) may be provided, such as a third electrode, a fourth electrode, and a fifth electrode. Each of the third, fourth and fifth electrode may serve as an anode or a cathode during operation of the stimulation device. In further examples, the cuff 215 may comprise a vibration device as disclosed in connection with figures 24-34. The vibraion device may, for example, comprise a piezoelectric element arranged to impart vibrations to the nerve 231, 232. The vibration device may be used instead of the electrodes E1, E2 or in combination with the electrodes E1, E2 and may, for example, be arranged to cause a portion of an inner surface of the cuff 215, which faces the tissue of the nerve, to reciprocate in a radial direction, i.e., back and forth towards and away from the nerve. In this way, vibrations may be imparted in the nerve to trigger action potentials to be generated (in case of the vibrational signal being an activation signal) or preventing action potentials to travel past the cuff 215 (in case of the vibrational signal being an inhibition signal, also referred to as a suppression signal or blocking signal). It will be appreciated that the above-described concept of activating / inhibiting the sympathetic / parasympathetic nerves 231, 232 may be employed to treat a variety of symptoms, depending on where in the body the stimulation device and the electrode arrangements 210, 220 are implanted and which effector tissue is innervated by the respective nerves 231, 232. In some examples, the nerves 231, 232 innervate smooth muscle tissue of the renal artery. This may allow the stimulation device to deliver stimulation signals inducing at least one of vasodilation and vasoconstriction in the renal artery, thereby affecting a blood pressure of the patient. In some examples, the first effector tissue forms part of an artery supplying erectile genital tissue with blood and the second effector tissue forms part of a vein draining the blood from the genital erectile tissue. This may allow the stimulation device to deliver stimulation signals for triggering or causing vasodilation in the artery and vasoconstriction in the vein, thereby inducing erection in the erectile genitalia. In some examples, the effector tissue 230 is smooth muscle tissue of a gastrointestinal tract of the patient. This allows the stimulation device to deliver stimulation signals affecting a level of motility of the gastrointestinal tract, thereby affecting at least one of nutrition uptake and fecal texture. In some examples, the effector tissue 230 is a glandular tissue, which allows the stimulation device to deliver stimulation signals affecting a level of glandular secretion of the glandular tissue 230. The stimulation device may hence be designed to stimulate various types of effector tissues in various parts of the body, depending on what type of response is desired and what type of symptom is treated. As various types of tissue (as well as individuals) may require various stimulation parameters, it may be beneficial to employ a calibration routine, in which the response to the applied stimulation signal is measured and used as feedback when controlling the stimulation parameters. However, some general observations may be made, which may serve as a starting point when choosing the stimulation parameters. For example, each type of tissue may be associated with a specific frequency range which may be used to trigger a response in the tissue. Muscle tissue is generally formed of muscle cells that are joined together in tissue that can be either striated or smooth. Striated muscle tissue is further classified as either skeletal or cardiac muscle tissue. Skeletal muscle tissue is typically subject to conscious control, whereas cardiac muscle tissue is typically found in the heart and not subject to voluntary control. The so-called smooth muscle tissue is a third type of tissue, which is typically neither striated in structure nor under voluntary control. The contraction of the muscle tissue may be activated through electrochemical nerve impulses, i.e., action potentials. The action potentials may result in the release of neurotransmitters, causing the muscle cell to contract. Smooth muscle cells may typically be activated, i.e., caused to contract, using a frequency in the range of 0.01 - 150 Hz. More specifically, the frequency may be in the ranges of 0.1 - 1 Hz, 1 - 10 Hz, 10 - 50 Hz and 50 - 150 Hz. It has been observed that a relatively low frequency component, such as pulse frequency, of about 1 Hz or less may be employed to imitate or enhance the slow wave potential associated with, e.g., pacemaker cells of the smooth muscle tissue. Furthermore, the pulse duration may be in the range of 0.01 - 100 ms, such as 0.1 - 4 mm, and preferably such as 1 - 5 ms. In case of an electric stimulation signal, the amplitude may be in the range of 0.1 - 15 mA, such as 0.5 - 5 mA. Furthermore, the separation between pulses, i.e., the pauses between adjacent pulses (or, in some cases, pulse trains) may be selected so as to match the wavelength of the natural pulses of the smooth muscle tissue. In different words, the distance between pulses of the stimulation signal may be selected to synchronize with the slow eave potential associated with, e.g., the pacemaker cells of the smooth muscle tissue. In other examples, the distance between the pulses may be selected to be slightly off the natural wavelength of the pulses of the smooth muscle tissue so as to drive a frequency of the natural pulses towards a higher frequency or a lower frequency. Skeletal muscle cells may typically be activated by means of a stimulation signal having a frequency of in a range of about 0.1 - 100 Hz, such as 1 - 10 Hz or 10 - 100 Hz. In an example, a frequency in a range of about 50 Hz may be used. Furthermore, a pulse duration in a range of 0.01 - 100 ms, such as 0.1 - 4 mm, and preferably such as 1 - 5 ms, may be employed. In case of an electric stimulation signal, the current amplitude may be in a range of 0.1 - 15 mA. In some examples, a desired muscle contraction response has been experimentally observed within a range of 0.5 - 5.0 mA. Cardiac muscle cells may typically be activated by slightly lower frequencies compared to skeletal muscle cells, such as in a range of 0.5 - 3 Hz. In an example, a beneficial response has been observed when applying a stimulation signal having a frequency of about 1 Hz. Similar to the skeletal muscles, the pulse duration may be in a range of 0.01 - 100 ms, such as 0.1 - 4 mm, and preferably such as 1 - 5 ms. In case of an electric stimulation signal, the current amplitude may be in a range of 0.1 - 15, such as 0.5 - 5.0 mA. Consequently, it will be appreciated that the stimulation parameters, such as frequency and amplitude, may be adapted to the muscle type and the type of response desired. This applies both to electric stimulation and vibrational stimulation signal. In the following, a detailed description will be given of a technology for electrically stimulating tissue, such as the above renal artery 20, for exercising the tissue and thereby improving the conditions for long term implantation. The body tends to react to a medical implant, partly because the implant is a foreign object, and partly because the implant interacts mechanically with tissue of the body. Exposing tissue to long-term engagement with, or pressure from, an implant may deprive the cells of oxygen and nutrients, which may lead to deterioration of the tissue, atrophy and eventually necrosis. The interaction between the implant and the tissue may also result in fibrosis, in which the implant becomes at least partially encapsulated in fibrous tissue. It is therefore desirable to stimulate or exercise the cells to stimulate blood flow and increase tolerance of the tissue for pressure from the implant. In the following, the use of electric signals for exercising tissue to improve the conditions for long term implantation will be described. It should be noted that there may be a difference between the electric stimulation signal (as well as the signal damping signal) discussed above in connection with for instance figure 1A, and the electric signal delivered for improving long term implantation conditions. While the former signal may be specifically adapted to trigger a muscular response for inducing vasodilation, the latter may be provided with the primary aim of preventing deterioration of the tissue and eventually necrosis of tissue of the renal artery. Preventing or reducing tissue deterioration does not necessarily require a stimulation causing the same degree of response as needed for inducing vasodilation. On the contrary, it may be advantageous to deliver an electric signal inducing a stimulation of the tissue stimulation (i.e., motoric response) without substantially affecting the flow resistance in the blood vessel. The “exercising” of the tissue to prevent deterioration may hence be combined with the stimulating causing vasodilation, and preferably cycled such that exercising cycles are performed between vasodilation cycles. The exercising, which thus may differ in effect or muscular response from the vasodilation, may be performed by delivering an exercising signal to the tissue via the electrode arrangements of the stimulation devices and / or damping devices discussed with reference to e.g. figures 1A, 3A, and 5A. It may be particularly advantageous to combine the exercising of the muscle tissue with medical devices comprising support structures, such as the cuff 115, 116 shown in figures 1F, 3C, 3F, 17A-D and the sensors in figures 21A-D. As these may form a relatively large contact surface with the tissue against which they are arranged, there is an increased risk for a negative impact on the health of the tissue. The electrical electrode arrangement and exercising methods described in the following may thus be implemented in any of the embodiments of the stimulation devices, signal damping devices, and sensors described above for the purpose of exercising the tissue which is in contact with such medical devices or implants. Figure 2A shows an example of a pulsed electrical signal to be applied to an electrode for electrically stimulating muscle tissue via an electrode-tissue interface, thereby exercising the muscle tissue, as discussed above. The electrical signal may be generated by a controller arranged outside the body or implanted in the. The characteristics of the electrical signal may be selected and varied determined on the electrical and properties at the electrode–tissue interface and on the actual response of the tissue. The electrical stimulation delivered to the muscle cells may depend on several factors, such as the configuration and placement of the electrode element at the tissue, the presence of fibrous material at the interface, the composition of the electrolyte in the interface, accumulation of non-conducting material on the electrode surfaces, etcetera. It is therefore suggested that the characteristics of the electric signal, as shown in the present figure, be selected and varied based on an observed or estimated response from the stimulated tissue. In the present example, the electrical signal is a pulsed signal comprising square waves PL1, PL2, PL3, PL4. However, other shapes of the pulses may be employed as well. The pulse signal may be periodic, as shown, or may be intermittent (i.e., multiple series of pulses separated by periods of no pulses). The pulses may have an amplitude A, which may be measured in volts, ampere or the like. Each of the pulses of the signal may have a pulse width D. Likewise, if the signal is periodic, the pulse signal may have a period F that corresponds to a frequency of the signal. Further, the pulses may be either positive or negative in relation to a reference. The pulse frequency may for example lie within the range of 0.01-150 hertz. More specifically, the pulse frequency may lie within at least one of the ranges of 0.1-1 Hz, 1-10 Hz, 10-50 Hz and 50-150 Hz. It has been observed that relatively low pulse frequencies may be employed to imitate or enhance the slow wave potential associated with pacemaker cells of the smooth muscle tissue. Thus, it may be advantageous to use relatively low pulse frequencies, such as 0.01-0.1 Hz or frequencies below 1 Hz or a few Hz for such applications. The pulse duration may for example lie within the range of 0.01-100 milliseconds, such as 0.1-20 milliseconds (ms), and preferably such as 1-5 ms. The natural muscle action potential has in some studies been observed to last about 2-4 ms, so it may be advantageous to use a pulse duration imitating that range. The amplitude may for example lie within the range of 1-15 milliamperes (mA), such as 0.5-5 mA in which range a particularly good muscle contraction response has been observed in some studies. In a preferred, specific example the electrical stimulation may hence be performed using a pulsed signal having a pulse frequency of 10 Hz, a pulse duration of 3 ms and an amplitude of 3 mA. In case a contraction of the smooth muscle tissue is desired, for example to cause vasoconstriction of a blood vessel or affect peristalsis in the gastrointestinal tract, it may be advantageous to select a separation between adjacent pulses based on the natural muscle action potentials or frequency of the natural muscle movements sometimes observed in smooth muscle tissue. A resonance approach, or standing wave approach, may thus be employed to amplify the movements or waves in the smooth muscle tissue. This may be achieved by matching pulse duration and / or separation with the corresponding parameters of the natural movements of the tissue. Fig.2B shows an example of a pulsed signal, comprising build-up period X1, in which the amplitude is gradually increasing, a stimulation period X2 during which the muscle tissue is exposed to a contracting stimulation signal, a ramp down period X3 in which the amplitude is gradually decreasing, and a stimulation pause X4 before a new build-up period is initiated. The build-up period may for example be 0.01-2 seconds, the stimulation period 1-60 seconds, the ramp-down period 0.01-2 seconds, and the stimulation pause 0.01-60 seconds. The pulse frequency may for example be 1-50 Hz, the pulse duration 0.1-10 milliseconds and the amplitude during the stimulation period be 1- 15 milliampere. The stimulation of skeletal muscle tissue may for example be performed using a frequency of 50 Hz and pulses having a duration of 100 μs. The current amplitude may be 1, 2.5, 7.5 or 10 mA. In particular, a desired muscle contraction response has been experimentally observed within a range of 0.5 to 5.0 mA. In the present example, a coiled electrode may be used as a cathode. Another example design is a multi-stranded wire arranged in a helical design. They can be imbricated in the muscular wall of the luminary organ, such as the renal artery 20, and can be stimulated in any desired pattern. The stimulus parameters may for example be biphasic pulses, 10 to 40 Hz, lasting 0.1 to 5 ms, with a current density of 3 to 5 mA / cm2. It may be beneficial to apply the stimulation with a preferred activation direction such that a majority of the action potentials generated in response to the stimulation propagate in the preferred activation direction. This may be achieved by inhibiting or blocking the nerve at a specific location such that no or at least only a minor part of the action potentials can travel beyond that location. For some applications, the preferred activation direction would be in the efferent direction, i.e., towards the effector tissue 230. Put differently, in some examples it may be beneficial if the application of the stimulation signal gives rise to action potentials propagating in the direction of the tissue in which the effector response is desired, rather than in the opposite, afferent direction (typically towards the CNS 233) to reduce adverse side effects of the application of the signal. Examples of adverse side effects include initiation of undesired or counter- productive feedback to the brain and can result in undesired sensations or activity of the patient. In some examples, it may be of interest to prevent action potentials from travelling in the efferent direction, i.e., away from the CNS 233 and towards the effector tissue 230. The generation of action potentials propagating in a preferred direction may be achieved by means of so-called unidirectional stimulation techniques, which will be described in the following with reference to the examples shown in Fig.3A to Fig.3F. The underlying rationale is based on the application of a suppression signal for suppressing action potentials propagating in the nerve in an undesired direction, typically the afferent direction (also referred to as antidromic direction). The suppression signal may comprise a frequency component for blocking, inhibiting, or suppressing the nerve’s conduction capacity in a similar manner as discussed above with reference to the inhibition signal. As mentioned above, such a frequency component may be relatively high, typically in the range of 1 - 10 kHz. The suppression signal, which may also be referred to as an inhibition signal, may be an electric signal or a mechanical (vibrational) signal. Combinations of the two are also possible, in which a combination of an electric signal and a vibrational signal is provided. The combined signal may, for example, be generated by a vibrational element, such as a piezoelectric element, comprising one or more electrodes 210, 220 for applying an electric signal. Vice versa, the combined signal may as well be generated by an electrode arrangement 210, 220 comprising a piezoelectric element for imparting vibrations into the nerve. A frequency of the inhibition signal may thus be selected to block or at least reduce the nerve’s ability to convey nerve signals. Therefore, the suppression signal may comprise one or more frequency components in the kilohertz range. Fig.3A is a schematic illustration of a system for affecting an effector response in effector tissue 230 of a patient according to some examples. The system comprises a stimulation device comprising a first electrode arrangement 210 for applying a stimulation signal to a nerve 231 innervating the effector tissue 230. The nerve may be a branch of the autonomous nervous system (ANS), such as sympathetic nerve or a parasympathetic nerve as discussed above in connection with the combined SNS and PNS stimulation. The stimulation device further comprises a second electrode arrangement 220 for delivering a suppression signal to the nerve 231 (the suppression signal may also be referred to as an inhibition signal). The second electrode arrangement 220 may be coupled to the nerve 231 at a position allowing afferent nerve signals, which are travelling towards the CNS 233, to be blocked or at least hindered. As indicated, the first electrode arrangement 210 and the second electrode arrangement 220 may be arranged spaced apart along a conduction direction of the nerve 231. The second electrode arrangement 220 may be coupled to the nerve 231 at a position between the first electrode arrangement 210 and the CNS 233. It will, however, be appreciated that the second electrode arrangement 220 in other examples may be coupled to the nerve 231 at a position between the first electrode arrangement 210 and the effector tissue 230 to suppress efferent nerve signals travelling towards the effector tissue 230. Afferent signals may refer to signals travelling towards the CNS 233. They typically originate from sensory receptors located throughout the body and carry sensory information from the body to the brain. The term “afferent” may hence be used to denote a propagation direction generally towards the CNS 233. Accordingly, efferent signals may refer to signals travelling in the opposite direction, away from the CNS 233 and towards various effector organs, such as muscles and glands. The efferent signals typically carry instructions from the CNS 233 and the brain to the body. The term “efferent” may hence be used to denote a propagation direction generally away from the CNS 233. The direction in which an electrical impulse travels along a neuron’s axon may also be described by the terms “antidromic” and “orthodromic” and may therefore be used to refer to the direction in which the action potentials, generated by the stimulation device, travel. Orthodromic conduction may be understood as referring to the propagation of nerve impulses in the natural, physiological direction. In a motor neuron, for example, this may be from the cell body (located in the spinal cord or brain) down the axon to the axon terminals that synapse with muscle fibers or other neurons (i.e., in the efferent direction). In a sensory neuron, it may be from the sensory endings towards the cell body and then onto the spinal cord or brain (i.e., in the afferent direction). Correspondingly, antidromic conduction may be understood as the direction of propagation of nerve impulses in the opposite direction to the normal or natural flow. For a motor neuron, this may mean an impulse travelling from the axon terminals back towards the cell body (i.e., in the afferent direction). In a sensory neuron, it may be from the CNS 233 out towards the sensory endings (i.e., in the efferent direction). It will be understood that the second electrode arrangement 220 may be employed to suppress nerve signals propagating in any of the above-mentioned directions, i.e., efferent, afferent, orthodromic, and antidromic direction, depending on the type of stimulation, the type of effector tissue, and what type of response is desired. The operation of the first electrode arrangement 210 and the second electrode arrangement 220, i.e., the generation and application of the stimulation signal and the suppression signal, respectively, may be controlled by a control unit 240 that is operably connected to the stimulation device. Further, the control unit may be configured to receive sensor input, such as from one or more sensors 250 arranged to generate a signal indicative of a response in the effector tissue 230 when stimulated by the stimulation signal. The stimulation device may hence be similarly configured as the stimulation device discussed above with reference to Fig.1A to Fig.1E. The control unit 240 may be configured to drive the stimulation device such that each of the first and second electrode arrangements 210, 220 are actuated in sequence. In an example, a delay of the suppression signal may be timed to generally match a conduction velocity of the stimulation signal in the nerve 231. The blocking or suppressed conduction of the nerve 231 can therefore be provided substantially at the same time when the action potentials, generated by the stimulation signal, reach the location where the suppression signal is applied to the nerve 231. In some examples, the control unit 240 may be configured to drive the stimulation device such that each of the first and second electrode arrangements 210, 220 apply the stimulation signal and the suppression signal substantially at the same time, such as concurrently (i.e., at least partly overlapping in time) or simultaneously. As mentioned above in connection with the stimulation of the SNS and PNS, the stimulation signal may be a low-frequency signal with a frequency in the range of, for example, 0.1 - 100 Hz and the suppression signal a high-frequency signal with a frequency in the range of, for example, 1 - 10 kHz. The first electrode arrangement 210 and / or the second electrode arrangement 220 may comprise a monopolar electrode delivering the stimulation signal and / or the suppression signal to the nerve 231. The monopolar electrode may be operated as an anode or a cathode, with a separate electrode forming a complementing cathode or anode for closing the electric circuit. This complementing electrode, closing the electric circuit, may be provided elsewhere, such as by a housing of the stimulation device, or may be arranged at another location in or on the patient’s body. In some examples, the first electrode arrangement 210 and / or the second electrode arrangement 220 may comprise a bipolar electrode, comprising a first electrode serving as a cathode and a second electrode serving as an anode for closing the electric circuit. A few examples will be discussed in the following with reference to the accompanying figures. Fig.3A illustrates a first electrode arrangement 210 and a second electrode arrangement 220 of a stimulation device according to some examples. The first electrode arrangement 210 comprises a first stimulation electrode 211 and a second stimulation electrode 212 for applying the stimulation signal to the nerve 231 (or, in some examples, directly to the effector tissue 230). The first stimulation electrode 211 and the second stimulation electrode 212 may be arranged spaced apart along the nerve such that the applied stimulation signal may propagate between the first and second stimulation electrodes 211, 212 in a conduction direction of the nerve 231. The first stimulation electrode 211 may hence serve as a cathode whereas the second stimulation electrode 212 may serve as an anode. Electrical leads, or conduction lines, may be coupled to each of the electrodes 211, 212 for supplying the respective electrode 211, 212 with electric power. The first electrode arrangement 210 may further comprise a cuff 215 configured to be at least partly arranged around the nerve 231 and hold the first electrode 211 and second electrode 212 in place against the nerve 231. Similar to the first electrode arrangement 210, the second electrode arrangement 220 may, in some examples, comprise a first suppression electrode 221 and a second suppression electrode 222 for applying the suppression signal to the nerve 231 (or, in some examples, directly to the effector tissue 230). The first suppression electrode 221 and the second suppression electrode 222 may be arranged spaced apart along the nerve 231. The first suppression electrode 221 may hence serve as a cathode, while the second suppression electrode 222 may serve as an anode during operation. Electrical leads, or conduction lines, may be coupled to each of the electrodes 221, 222 for supplying the respective electrode 221, 222 with electric power. The second electrode arrangement 220 may further comprise a cuff 225 configured to be at least partly arranged around the nerve 231 and hold the first suppression electrode 221 and second suppression electrode 222 in place against the nerve 231. In other examples, the electrodes 211, 212, 221, 222 may be replaced with vibration elements, such as piezoelectric elements, for providing a mechanical (vibrational) signal to the nerve 231. It will be appreciated that further electrodes may be provided to deliver the stimulation signal and the suppression signal, respectively. An example of such a configuration is shown in Fig.3B and C, illustrating a cuff electrode arrangement 210, 220 which can be used to deliver the stimulation signal and / or the suppression signal. Each cuff electrode 210 shown in the present example includes a first electrode 211, a second electrode 212, and a third electrode 213. Each of the electrodes 211, 212, 213 may comprise an electrically conductive surface configured to be arranged to abut or rest against the tissue to which the electrical signal is to be delivered. The electrodes 211, 212, 213 may be individually controlled electrically. At least a first one of the electrodes 211, 212, 213 may be operated as a cathode, wherein at least a second one of the electrodes 211, 212, 213 may be operated as an anode for delivering the stimulation signal or the suppression signal to the nerve 231. In this arrangement, the electrode arrangements 210 may comprise a lead 216 for providing the electric power required for the stimulation signal / suppression signal. The lead may be oriented across the nerve 231 or along the nerve 231, depending on the implantation site and the available space at the nerve 231. The cuff electrode 210 in figure 3C may comprise a body 215 which may be molded from an elastomeric material (e.g., silicone). The electrodes 211, 212, 213 may be integrated with the body 215 during the molding process. The body 215 may be shaped or formed to normally assume a curled or tubular spiral or rolled configuration. As shown, the body 215 may in its normal, coiled condition have overlapping end portions forming a spiral which extends more than 360° end to end. The body 215 may be elastically uncoiled to increase its inner diameter and allow the cuff electrode 210 to be initially fitted about a periphery of a target nerve 231. Further, the coiled shape of the body 215 allows for the inner diameter of the cuff electrode 215 to be further adjusted to post-operative changes that might occur for example due to swelling. The elasticity of the body 215 may beneficially wrap the electrodes 211, 212, 213 snugly against the periphery of the nerve 231. Fig.3D and Fig.3E show examples of an electrically conductive surface, or electrode 211, of an electrode arrangement 210, 220 as mentioned above. The electrode 211 may be formed by a single, continuous conductive surface as in Fig.3D or a surface that is segmented into separate conductive segments that may be electrically coupled by a wire or conductive lead as in Fig.3E. A lead 217 may be provided to power the electrode 211. Fig.3F shows an example wherein the cuff electrode 210 is wrapped around the target nerve 231 such that the electrically conductive surfaces, forming the stimulation electrode(s) or the suppression electrode(s), make and sustain circumferential contact substantially about the entire periphery of the target nerve 231. It will, however, be appreciated that in some examples the electrode(s) may be positioned to make contact with the target nerve 231 along the length axis of the nerve 231, i.e., the propagation direction of the nerve 231. The conductive surfaces, which form the stimulation / suppression electrodes, may be made from strips of metal, such as platinum. In some examples, they may be formed from a thin film of metal, which may be deposited on a surface of the body 215 forming the cuff of the electrode arrangement 210, 220. In an example, each of the conductive surfaces (or strips) may measure about 10 mm in length and 2 mm in width. It will be appreciated that in further examples, not illustrated, one or more of the electrode arrangements 210, 220 may have a configuration different from the cuff electrode design. The electrode arrangements 210, 220 may, for example, be configured to be placed against the nerve 231 without encircling or enclosing it. The electrode arrangements 210, 220 may be configured as needle electrodes arranged to protrude into the nerve 231 or lie against an outer surface of the nerve 231. In further examples, the electrode arrangements 210, 220 may be patch electrodes similar to the ones illustrated in Fig.1B and Fig.1C. The effector response may be measured by a sensor device, such as the sensor device 250 shown in the example of Fig.1A and Fig.3A. The use and operation of such a sensor device 250 will be described in the following with reference to Fig.5A to Fig.5D. Figure 4A is a diagram illustrating a signal damping mechanism, or phase cancellation mechanism, according to some embodiments. In some example, the mechanism may also be referred to as a nerve inhibition or blocking mechanism, in which action potentials are hindered from propagating past an application point of the damping signal. This may be a way of achieving unidirectional stimulation, in which the stimulation signal is delivered in a preferred direction in of the nerve. Figure 4A schematically shows an electric stimulation signal comprising a series of positive pulses PL1, and an electric damping signal comprising a series of negative pulses PL2. The stimulation signal may originate from a stimulation device 110 arranged to cause vasodilation in the renal artery 20, whereas the electric damping signal may be generated by a signal damping device 120, comprising a control unit which may be arranged outside the body or be implanted in the body. Other applications are however possible, such as electric stimulation of effector tissue in general. Examples of such tissue include smooth muscle tissue, skeletal tissue, and glands. For illustrative purposes, however, the signal damping or blocking concept will be explained by means of the particular example of vasodilation in the renal artery. The control unit may be operatively connected to an electrode arrangement by means of one or several leads. The electrode arrangement may comprise a plurality of electrode elements attached to the muscle tissue of the renal artery wall 20, to tissue in close vicinity of the muscle tissue of the renal artery, or a nerve innervating the renal artery, such that the electrode elements are allowed to deliver the damping signal to said tissue. The electrical signals shown in the present figure may either reflect the signal as generated at the stimulation device and signal damping device, respectively, or the signal as delivered to the tissue. In the present example, the electrical signals are pulsed signals comprising square waves PL1, PL2. However, this may be considered to represent an ideal signal, and it is appreciated that other shapes of the pulses may be provided as well. The pulse signals may be periodic, as shown, or intermittent (i.e., multiple series of pulses separated by periods of no pulses). The pulses may have an amplitude A1, A2, which may be measured in volts, amperes, or the like. Each of the pulses of the signals may have a pulse width D1, D2. Likewise, if the signal is periodic, the pulsed signals may have a period F1, F2 that corresponds to a frequency of the signal. Further, the pulses may be either positive or negative in relation to a reference. In the present example, the signal originating from the propagating stimulation signal may comprise positive pulses PL1 whereas the damping signal may comprise negative pulses PL2. In the present example, the electric stimulation signal may be a pulsed signal comprising square waves having a frequency in the range of 0.01-150 Hertz. The pulse duration may lie within the range of 0.01-100 milliseconds (ms), such as 0.1-20 ms, and preferably such as 1-6 ms. The natural muscle action potential has in some studies been observed to last about 2-4 ms, so it may be advantageous to use a pulse duration imitating that range when stimulating the tissue to cause it to relax. The amplitude of the stimulation signal may for example lie within the range of 1-15 milliamperes (mA), such as 0.5-5 mA, in which range a particularly good muscle response has been observed in some studies. In a preferred, specific example, the electrical stimulation delivered by the stimulation device 120 may hence be performed using a pulsed signal having a pulse frequency of 10 Hz, a pulse duration of 3 ms and an amplitude of 3 mA. The pulsed signal shown in figure 4A (in solid lines) may be considered to represent the characteristics of such a stimulation signal as it is propagating through the tissue of the renal artery 20. The damping signal (indicated by dashed lines) may be designed to counteract, or mitigate, the tissue’s response to the stimulation signal. In the example shown in the present figure, this may for instance be achieved by providing a series of pulses PL2 having a polarity that is reversed in relation to the pulses PL1 of the signal originating from the stimulation signal. Further, the damping signal may be phase shifted in relation to the positive pulses. The timing of the signals may hence be selected such that the negative pulses PL2 are positioned at the time of the positive peaks PL1, or slightly delayed relative the positive peaks PL1, as indicated in figure 4A. A negative pulse PL2 may be delivered to the tissue shortly after the positive pulse, before the cells have had time to react to the stimuli provided by the positive pulse. Put differently, the damping signal may be delivered to the cells at the onset of the change in cell polarization, thereby reducing or cancelling cell polarization. The negative pulse PL2 may thus act to counteract, or cancel, the stimuli provided by the positive pulse PL1, thereby preventing the cells from contract, or at least reducing the contraction triggered by the positive pulse PL1. It should be understood that the signals illustrated in the above example are schematic and ideal, and not necessarily a true representation of the actual signals delivered to the tissue. The actual signals may be more complex, having a more complex frequency composition and comprising various degrees of noise. The illustration in figure 4A is purposely simplified to help elucidate the inventive concept of applying a damping signal to counteract or reduce the effects of the stimulation signal as it propagates to other parts of the body which are not the primary target of the stimulation. It may therefore be advantageous to provide a sensor measuring the signal, which is to be damped or counteracted, and design the damping signal based on input from the sensor. This allows for the damping signal to be generated also in cases where the stimulation signal varies over time or is difficult to estimate or model. By such a feedback loop, a more flexible damping may be provided. As mentioned above, the signals do not necessarily have to be formed of pulses or square waves. Figure 4B illustrates another (still simplified) example, wherein the signal originating from the stimulation signal is shaped as a sine wave, and wherein the damping signal has a corresponding shape and is phase shifted to counteract or cancel the stimulation signal. Other signal shapes are however equally possible, including square, triangle and sawtooth waves and combination thereof. A further example is shown in figure 4C, in which the damping signal is configured to disturb or “scramble” the signal originating from the stimulation device 110 such that it has a reduced effect on tissue arranged remote from the electrode elements 112a of the stimulation device 110. The damping signal may for instance comprise a frequency which is higher than the frequency of the signal from the stimulation device 110, such that the resulting, superposed signal that reaches the individual tissue cells are less suitable for triggering a contraction of the smooth muscle tissue cells or a conveying of the stimulation signal by the nervous tissue cells. This is based on the observation that a stimulating signal may have a reduced impact on cells when the frequency is outside a certain interval. Put differently, the stimulation of tissue may be less efficient for higher frequencies, and the damping signal may therefore be applied to increase the frequency accordingly. Fig.5A is a schematic illustration of a stimulation device configured to deliver a stimulation signal to a nerve 231 innervating an effector tissue 230 of a patient. The stimulation device may form part of a system comprising a sensor device 250, configured to generate a sensor signal indicating the effector response in the effector tissue 230, as well as a control unit or controller 240, operable to receive the sensor signal and control an operation of the stimulation device based at least in part on the sensor signal. The nerve 231 may be a sympathetic nerve or a parasympathetic nerve extending between the central nervous system 233 and the effector tissue 230, as previously discussed in connection with Fig.1A and Fig.2A. Consequently, the stimulation signal may be an activation signal, such as the previously discussed low-frequency signal, or an inhibition signal, such as the previously discussed high-frequency signal. For illustrative purposes, the stimulation signal is applied by means of an signal generating means, such as an electrode arrangement 210 arranged to touch the nerve 231. The exemplary electrode arrangement 210 may be a unipolar electrode, comprising a first stimulation electrode 211 that may act as a cathode or anode. Another electrode (not shown) may be provided elsewhere to close the electric circuit. This circuit-closing electrode may, for example, be formed by a portion of a housing of the stimulation device. It will however be appreciated that other configurations of the stimulation device and the electrode arrangement(s) 210 are possible. The sensor device 250 may be configured to measure the effector response in various ways. The sensor device 250 may be configured to employ one or more electrodes for measuring an electrical characteristic of the effector tissue 230. In further examples, the sensor device 250 may be configured to employ one or more mechanical sensor elements for measuring a mechanical characteristic or response in the effector tissue 230. The information provided by the sensor device 250 may thus be used to determine or monitor an activity or response in the effector tissue 230 and provide feedback that can be used for controlling the operation of the stimulation device. Fig.5B shows an example in which the sensor device 250 comprises one or more sensor electrodes 251, 252 configured to measure an electric activity in the effector tissue 230 in response to the mechanical or electrical stimulation signal. This approach may be referred to as electromyography (EMG). The electrode(s) may be arranged to measure the electric activity in the effector tissue 230 (typically muscle tissue). An increased activity in the effector tissue 230 may typically cause an increased electrical activity, whereas the effector tissue 230 normally does not produce any electrical activity during rest. Therefore, EMG may be used to detect and quantify changes in the electrical activity of the effector tissue 230 caused by an applied stimulation signal. In the present example, a first sensor electrode 251 and a second sensor electrode 252 are provided to generate the sensor signal. The voltage signal, which indicates the response in the effector tissue 230, may typically be in the range of 1 - 2 mV. Fig.5C shows an example in which the sensor device 250 comprises one or more sensor electrodes 251, 252, 253, 254 configured to measure a change in electrical impedance in the effector tissue in response to the stimulation signal. This approach may be referred to as electrical impedance myography(EIM). The electrodes may be arranged to apply an electric signal I, typically in the kHz to MHz frequency range, to the tissue 230 and measure the resulting voltages. The sensor device 250 may, in some examples, comprise a first electrode 251 and a second electrode 252 for applying the electric signal I and a third electrode 253 and a fourth electrode 254 for measuring the resulting voltage V. This information may be used to determine the impedance, which may be separated into a resistance and reactance. For a given resistance and reactance, a phase may be calculated. It has been found that all three parameters, i.e., resistance, reactance, and phase, may be indicative of the effector response caused by the stimulation signal delivered by the stimulation device. The impedance of the effector tissue 230 may, for example, be measured during the stimulation and when no stimulation signal is applied. Differences in impedance when the tissue 230 is stimulated and when not stimulated may be used to analyze the effects of the stimulation and control the operation of the stimulation device accordingly. In the present examples, the electrodes are arranged spaced apart on a surface of the effector tissue 230, with the third and fourth electrodes 253, 254 arranged between the first and second electrodes 251, 252. In some examples, a typical impedance over a muscle is about 1 kΩ and the measured changes in response to the stimulation are in the order of 1 Ω. Thus, by measuring impedance variations of about 0.1 %, information may be retrieved about the muscle’s response to the applied stimulation signal. Combinations of the EMG and EIM approaches are possible. Thus, in some examples, the sensor device 250 comprises an electromyographic sensor configured to measure an electric activity in the effector tissue 230 and an electric impedance sensor configured to measure a change in electrical impedance in the effector tissue 230. The control unit 240 may be configured to receive sensor signals from both the electromyographic sensor and the impedance sensor and control or adjust the application of the stimulation signal based on the received sensor signals. The combination of EMG and EIM may be beneficial because it may enhance the reliability of muscle contraction detection. In this example, EMG may provide detailed information on muscle activity, while EIM may offer insights into muscle composition and health. When used together, they may compensate for each other’s limitations, improving the accuracy and robustness of effector response monitoring. This synergy may be particularly advantageous in environments with potential for mechanical disturbances to the electrodes, ensuring more consistent and reliable effector response readings. The sensor electrode 251 - 254 of the sensor device 250 may be configured to be arranged at the effector tissue 230 or inserted into the effector tissue 230. The sensor electrode(s) 251 may in some examples be formed as one or more patch electrodes that can be attached to the effector tissue 230. In some examples, the sensor electrode(s) 251 may be formed as needle electrodes arranged to protrude at least partially into the effector tissue 230. The sensor device 250 may further comprise a reference electrode allowing the sensor signal to be based on an electrical interaction between one or more sensor electrode 251 and the reference electrode. The reference electrode may be formed by a housing of the stimulation device and / or an electrode arranged at the effector tissue 230, spaced apart from the sensor electrode 211. As mentioned above, the sensor device 250 may in some examples comprise one or more mechanical sensor elements for measuring a mechanical characteristics or response. The sensor device 250 may, for example, be configured to measure mechanical movement in the effector tissue 230. Fig.5D shows an example of such a sensor device 250 which comprises a strain gauge for measuring a contraction or relaxation of effector tissue 230 in response to the stimulation signal. Thus, the effector tissue 230 may be muscle tissue, such as smooth tissue. The strain may be positive (due to elongation of the muscle tissue) or negative (compressive, due to contraction of the muscle tissue). The strain gauge may be arranged to convert a change in dimension to a change in electrical resistance. In the present example, the strain gauge comprises a wire or foil 256 arranged in a grid pattern. During operation, the electrical resistance of the strain gauge may change in proportion to the deformation (and thus strain) experienced by the wire or foil pattern 256. An excitation voltage may be applied to the strain gauge and a sense voltage may be measured as an output voltage. As the resistance changes due to induced strain, the output voltage also changes. The present example comprises a metallic foil pattern 256 arranged on a flexible support 255, such as a thin silicone film 255. The flexible support or support patch 255, can be attached to an outer surface of the effector tissue 230 to be measured. Due to the flexible nature of the support 255, it may deform and contract as the effector tissue 230 deforms and contracts, thereby causing the metallic foil pattern 256 to deform accordingly. The output from the sensor device 250 may be retrieved by the control unit 240, which may be configured to determine a response measure based on the sensor signal. The response measure may be understood as a measure indicative of the effector response. Hence, the response measure may be a certain voltage, impedance, phase, resistance, or degree of contraction or relaxation, depending on the principle of operation used by the sensor device. In case of the sensor device 250 being an EMG sensor, the response measure may be a voltage, in case of the sensor device 250 being an EIM sensor, the response measure may be an impedance and / or phase, and in case of the sensor device 250 being an mechanomyography (MMG) sensor, the response measure may be a resistance or degree of deformation. The control unit 240 may be operable to compare the response measure with a predetermined reference measure and control the stimulation device based on the comparison in order to adjust or maintain a desired response in the effector tissue 230. The control unit 240 may, for example, increase an intensity of the stimulation signal in response to the response measure being below the reference measure and reduce the intensity of the stimulation signal in response to the response measure exceeding the reference measure. The control unit 240 may thus operate as a closed-loop controller, or feedback controller, using information carried by the sensor signal as feedback when controlling the operation of the stimulation device in a control loop. The control unit 240 may be configured to increase the intensity of the stimulation signal by increasing at least one of a frequency, current amplitude, and voltage amplitude of the stimulation signal. Further, the control unit 240 may be configured to reduce the intensity of the stimulation signal by reducing at least one of the frequency, current amplitude, and voltage amplitude of the stimulation signal. The predetermined reference measure may be based on a previous measurement of the effector response in the patient and / or on previous measurements of effector responses in other patients. The control unit 240 may be configured to monitor the level of effector response over time and control the stimulation device based on a change rate in the effector response over time. Thus, the control unit 240 may be arranged to calculate a time derivative of the effector response and control the operation of the stimulation device accordingly. It will be appreciated that the response measure in some examples may be used to determine a calibration parameter of the stimulation device. The determination of the calibration parameter may form part of a calibration process, which may be performed in connection with implantation of the stimulation device. The calibration process may also be performed intermittently or on a regular basis, for example upon request by a healthcare professional. The calibration parameter may indicate an offset needed to adjust a characteristic of the stimulation signal, such as a voltage, frequency, or current, to achieve a desired level of effector response. The calibration process may hence be performed to ensure proper operation of the stimulation device and increase the prospects of a desired and predictable effect of the applied stimulation signal. Figure 6 is a schematic outline of a device, or system, for affecting an effector response in a patient. In a particular example, the system may be used for treating a patient with hypertension. The system may comprise an implantable stimulation device 110 and, optionally, an implantable signal damping device 120, which may be similarly configured as the stimulation and signal damping devices discussed above in connection with the previous examples. The system may further comprise an implantable source of energy, or energy storage unit 130, for energizing the stimulation device 110 and the signal damping device 120 and providing the electrical energy required for generating the electrical stimulation signal and the electric damping signal. Further, the system may comprise a control unit or controller 150 configured to control the generation of the stimulation signal and / or the damping signal, and a sensor configured to generate input that can be used for generating the damping signal. Any of the above elements, such as the energy storage unit 130, the sensor 140, and the controller 150, or parts thereof, may be configured to be attached to a tissue wall of the body by means of a holding device. The energy storage unit 130 may for instance be of a non-rechargeable type, such as a primary cell, or of a rechargeable type, such as a secondary cell. The energy storage unit 130 may be rechargeable by energy transmitted from outside the body, from an external energy storage unit, or be replaced by surgery when needed. The controller 150 may comprise an electric pulse generator for generating electrical pulses to the stimulation signal and / or the damping signal. The controller 150 may be integrated with the energy storage unit 130 or provided as a separate, physically distinct unit which may be configured to be implanted in the body or operate from the outside of the body. In case of the latter, it may be advantageous to allow an external control unit to communicate wirelessly with the controller 150 for example by means of a communication unit of a more general controller (not shown). The external controller may for example be a wireless remote control, and the controller may in such cases advantageously comprise an internal signal transceiver configured to receive and transmit communication signals from / to an external signal transmitter. More detailed examples are disclosed in connection with figures 35A-U. In some examples, the controller 150 may be configured to generate a signal indicating a functional status of the source of energy 130, such as for instance a charge level or a temperature of the source of energy 130. Further, the control unit 150 may in some examples be configured to indicate a temperature of at least one of the stimulation device 110, the signal damping device 120 and tissue adjacent to the stimulation device 110 or the signal damping device 120. In some cases, the system comprises a sensor 140, which may be configured to sense a physical parameter of the body and / or the implantable device. The sensor may be similarly configured as the sensors discussed below in connection with figures 21A-D. The sensor 140 may for example be employed to sense or detect an effector response in the form of a relaxation or contraction of muscle tissue. This may, for example, include a stretching or contraction of the outer wall of a renal artery 20, thereby allowing for the vasoconstriction and vasodilation of the renal artery 20 to be monitored. The sensor 140 may in this example comprise a strain gauge, as shown in figure 21D, configured to indicate a strain of the outer wall of the renal artery 20. In an example, the relaxation of the blood vessel may be verified by means of the sensor 140 and the stimulation device 110 controlled accordingly. The stimulation device 110 may for example modify the stimulation signal based on feedback from the sensor 140 pertaining to the muscular response to the stimulation signal, which advantageously may allow for the stimulation signal to be modified to improve or increase the vasodilation in the renal artery 20. In further examples, the sensor 140 may comprise a pressure sensor configured to generate a signal indicating a pressure in the renal artery 20. The signal indicating the pressure in the blood vessel may for instance be sent to the controller 150 and used as input for adjusting the electrical stimulation signal affecting the vasomotor tone of the smooth muscle tissue of the renal artery 20. In further examples, the sensor 140 may be configured to generate a signal indicative of electrical properties of the signal propagating from the stimulation device 110, such as the signal propagating towards regions of the body which should not be stimulated by the stimulation signal. Examples of such regions may for instance include the aorta 22 and ganglia from which the nerves innervating the renal artery origin. The sensor 140 may for example include a voltage sensor and / or a current sensor and may be configured to deliver information to the controller 150 pertaining to for instance voltage, amplitude and frequency of signals propagating from the electrode elements 112a of the stimulation device 110. The controller 150 may be configured to use this information to generate a damping signal which can be supplied to for instance the tissue of the renal artery, close to the bifurcation with the aorta, or at least reducing the tissue’s muscular response to the propagated stimulation signal. The sensor may for example be structurally integrated with the signal damping device 120, or provided as a separate, structurally distinct unit. In some examples, the sensor may comprise one or several electrode elements or electrical probes, which may be arranged to engage the nerve or muscular tissue through which the signal from the stimulation device passes. In some examples, the sensor 140 may be configured to sense or detect action potentials that are being transmitted to the muscle tissue. The action potentials may be registered by the sensor 140 and information relating to the action potentials be transmitted to the controller 150. The controller 150 may use the received information when controlling the signal damping device 120 to reduce the effect of the electric stimulation signal on tissue to which the electrical stimulation signal has propagated. As mentioned above in connection with figure 6 it will be appreciated that any of the above embodiments, may include a sensor configured to generate a signal indicative of an effector response of the patient. In particular examples, the effector response may be a vasodilation or vasoconstriction, affecting a blood pressure (or vascular resistance) of the patient. The various examples and embodiments of sensors described herein may be combined with any of the systems and devices for delivering a stimulation signal as disclosed herein. Similar features and effects will therefore not be repeated in the following. The inventive concept may utilize sensors of a transducer type, in which energy is converted from one form to another. The sensor may thus be configured to convert a pressure signal (measured directly in the blood or indirectly via an intermediate medium, such as the wall of the blood vessel) into for instance an electrical signal which thus may be considered to be a function of the pressure. The sensor may be of a dynamic type, configured to capture or monitor the pressure over time and generate a signal indicating the pressure for each measurement point (or continuously, depending on sensor type). The control unit, to which the signal may be sent, may then analyses the signal and make the decision to initiate or stop the stimulation of the renal artery. Alternatively, the sensor may be of a switch type which is configured to turn on or off at a particular pressure. For example, the sensor may be configured to generate a trigger signal for blood pressures being above a certain threshold (or, in alternative configurations, for blood pressures being below a certain threshold). In such cases, the control unit may be configured to treat the signal as a trigger or ON signal, initiating the stimulation of the muscle tissue of the renal artery. In different words, the values of the signal from the sensor may either be (substantially) continuous (giving a substantially true representation of any changes in the measured quantity) or binary, indicating whether the measured quantity is above or below a given limit. The sensor may be configured to measure the pressure relative to a reference pressure, such as perfect vacuum. This type of sensor may be referred to as an absolute pressure sensor. The sensor may also be a differential pressure sensor, configured to measure the difference between two pressures, such as the pressure inside the blood vessel compared to the pressure outside the blood vessel, or the atmospheric pressure. This type of sensor is sometimes referred to as a gauge pressure sensor. The pressure sensor may be of a force collector type, using a force collector (such as a diaphragm, piston, bourdon type, or bellows) to measure strain (or deflection) due to applied force over an area (pressure). The sensor may for example utilize piezoelectric or piezoresistive effects to detect strain due to applied pressure or employ a variable capacitor technology to generate a signal as pressure deforms for instance a diaphragm. Pressure induced displacements of elements of the sensor (or parts of the patient’s body) may also be measured by means of changes in inductance, Hall effect, eddy currents and the like. In further examples, electrically conductive strain gauges may be attached to an area which moves due to applied pressure and used for generating a signal indicative of the movement of the area. In yet further examples the sensor may operate based on an optical technique, including the use of the physical change of an optical fiber to detect strain due to applied pressure or optical coupling. Alternatively, or additionally, changes in the blood flow may be measured using optical methods, involving for instance radar or doppler effects, or by monitoring the optical coupling efficiency of light passing through the blood vessel. These principles may utilize the observations that light may behave differently depending on the pressure in the blood. Non-limiting details and examples will be discussed in further detail in the following. The sensor may be arranged at the renal artery, preferably the same renal artery as the one to which the electrical muscle tissue stimulation is applied. A merit of this arrangement is that the sensor may deliver a signal indicating pressure changes resulting from vasodilation of the renal artery and can therefore be considered to provide a more direct feedback to the stimulation process. Put differently, a control loop may be achieved, which utilizes feedback data that are obtained from the same blood vessel as the one that is being electrically stimulated. Alternatively, or additionally, a sensor may be arranged elsewhere, i.e., remote from the renal artery which is electrically stimulated. One or more sensors may hence be arranged at a blood vessel in another part of the patient’s body, such as the aorta, or an artery in the abdomen or a limb of the body, to generate a signal indicative of a systemic blood pressure of the patient. It may be advantageous to arrange the sensor at a position which is easier to access than the renal artery, allowing for the sensor to be implanted in a less complicated and invasive surgical procedure. The sensor may be configured for long-term implantation, or permanent implantation, in which the sensor is expected to be operating for several months or years without having to be replaced or physically accessed. This allows for the sensor to be operable continuously during the operation of the stimulation device. Alternatively, the sensor may be configured for a temporal use, for instance during a shorter period in which the stimulation device is calibrated. The sensor may thus be implanted for a few hours, days or weeks, for example during setup or calibration of the stimulation device, whereafter the sensor may be removed. According to some embodiments, the sensor may be arranged to measure the pressure directly in the blood vessel. This may for example be achieved by arranging a probe inside the blood vessel, such as the renal artery, or another artery such as the radial artery, femoral, dorsalis pedis or brachial artery. The probe may thus be employed to generate a signal indicative of the pressure acting on the probe, thereby giving an indication of the blood pressure. According to some embodiments, the pressure sensor may be arranged at an outer wall of the blood vessel of the patient. The sensor may for example be formed as a cuff at least partly enclosing the blood vessel or be arranged to abut at least a portion of the outer wall. By this arrangement, the sensor may be configured to measure pulse waves transmitted by the blood into the wall of the blood vessel. The pulse waves transmitted through the wall may be converted into a signal, such as an electrical signal, by means of a strain gauge reacting on a strain induced in the wall portion by the pressure pulses, or by means of a contact pressure sensor configured to react or monitor a contact pressure between the outer wall portion and the sensor. A pulse wave, transmitted through the blood, may hence give rise to an increased pressing force between the outer wall of the blood vessel and the pressure sensor, which in turn may be configured to convert the increased pressing force into a signal indicative of the pressure according to a technique mentioned above. According to some embodiments, the sensor may comprise a light source configured to input light into the blood, such as through the wall portion of the blood vessel, and a light sensor configured to receive light transmitted from the light source. The light sensor may for instance be arranged outside the blood vessel, at a side opposing the light source. This may be referred to as an optical sensor, which in some examples may base the pressure measurements on a light coupling efficiency through the blood vessel. The light coupling efficiency may for instance be a function of a contact pressure between the light source and the wall portion of the blood vessel, and / or a contact pressure between the light sensor and a wall portion of the blood vessel and may therefore be used to indicate a characteristic of the pressure pulse generated by the heartbeats. Optical methods may also be used to measure a deflection, or movement, of a wall portion of the blood vessel in response to the pressure pulse wave travelling through the blood vessel. Such an optical method may for instance utilize the doppler radar effect to monitor a pulse wave causing a movement in the wall portion of the blood vessel. According to some embodiments, the sensor may operate according to the auscultatory principle, in which a constrictive element, or constriction device, is placed around the blood vessel and operated to constrict the blood vessel until is occluded and the blood flow therein stopped. The constriction may then be gradually released, and the constrictive pressure registered as a function of the returning blood flow. In an example, the constriction device is used in an oscillometric method, in which oscillations in the constrictive pressure caused by oscillations in the blood flow, i.e., the pulse, are measured. The constriction device may for instance be operated to a pressure initially exceeding the systolic arterial pressure and then reduce to below the diastolic pressure. When blood flow is substantially nil (constrictive pressure exceeding systolic pressure) or substantially unimpeded (constrictive pressure below diastolic pressure), the constrictive pressure may be essentially constant. When blood flow is present, but restricted, the constrictive pressure, which may be monitored by the sensor, may vary periodically in synchrony with the cyclic expansion and contraction of the blood vessel, i.e., it will oscillate. Over the release period, in which the constrictive pressure is reduced, the recorded pressure waveform may form a signal from which the oscillometric pulses may be extracted using a bandpass filter. The extracted oscillometric pulses may form a signal referred to as the oscillometric waveform, OMW, which can be analyzed and processed to estimate the systolic, diastolic and mean arterial pressure. The sensor may in some examples be configured to generate a signal indicative of a vascular resistance of a blood vessel of the patient. As the blood pressure may be understood as a function of (inter alia) the vascular resistance, this measure may be used when estimating the blood pressure. The sensor may for instance be configured to measure a flow of blood in the blood vessel, to measure a vasodilation or vasoconstriction of the blood vessel, and / or a size of the blood vessel (such as inner or outer diameter or cross-sectional size). The blood flow through the blood vessel may for instance be monitored by means of a light coupling method as indicated above, where the composition of the blood is monitored to estimate a flow of the blood. This may for example involve observing or estimating a number of red blood cells passing a certain region or volume of the blood cell per unit of time. An increase in blood flow may indicate a reduced vascular resistance, whereas a reduced blood flow may indicate an increased vascular resistance. A printed circuit board (PCB) 260, may be employed to accommodate the circuitry and electrical components enabling the functionality of the systems described above. Accordingly, at least one of the stimulation device, the source of energy, and the control unit 240 may be supported by such a PCB. The PCB may be integrated in a housing or casing facilitating implantation in the body of the patient. Specific examples of PCBs 260 will now be discussed with reference to Fig.7A and B. The PCB 260 serves as a physical platform for supporting and interconnecting electronic components of the system. The PCB 260 typically comprises a substrate 263 on which conductive paths 261 are etched or printed to establish electrical connections. Components such as resistors, capacitors, and integrated circuits such as ASICs may then be mounted on the substrate 263. The design and configuration of the PCB 260 depend on the intended application and site of implantation, with considerations for size and flexibility playing roles. Fig.7A shows an example of a multi-layer PCB 260, in which a plurality of substrate layers 263, each provided with its own set of conductive paths 261, are bonded together with layers of insulation. The multi-layer configuration reduces the footprint of the PCB 260, allowing for more functionality within the limited space of a medical implant, such as the stimulation device. The layers 263 are interconnected through vias 262 which may be through-holes filled or plated with conductive material. The relatively compact design of the PCB 260, with the reduced footprint enabled by the multi-layered configuration, makes it possible to implant the device in locations where the available space is relatively restricted. The PCB 260 may also be of a flexible type and / or a stretchable type. Flexible PCBs are typically made using a flexible substrate, such as polyimide or polyester film, which allows the PCB to conform to a specific shape or flex during its use. This flexibility is particularly advantageous in medical implants that need to move or flex with the surrounding tissue, reducing the risk of damage to both the device and the tissue. Flexible PCBs can be single-layered or multi-layered and may, beneficially, be used in implants requiring adaptability to movement or specific anatomic contours. Stretchable PCBs may be fabricated from materials that can withstand stretching, such as silicone-based substrates with conductive paths that can withstand stretching. The conductive paths may, for example, be formed of silver-filled silicone, or a conductive path or wire may be arranged in a ‘serpentine’ trace. The serpentine trace may be characterized by its zigzag or wave-like pattern, effectively distributing mechanical stress over a larger area and absorbing deformations caused by the substrate moving or stretching. Fig.7B shows a particular example of a PCB 260 which is both flexible and stretchable. The PCB 260 comprises one or more flexible portions, such as flexible substrate portions 263, as well as one or more flexible portions comprising a stretchable substrate 264 with a conductive path 265 arranged in a wave-like pattern. In the present example, the PCB 260 comprises three flexible portions 263 interconnected by two stretchable substrate portions 264. The resulting arrangement is a PCB 260 that can conform to the specific shape of the tissue to which it is attached and adapt to movements, such as contractions of the tissue. In further examples, two or more non- flexible portions (such as regular planar PCB portions or multi-layered PCB portions) may be interconnected by one or more flexible or stretchable portions to provide some flexibility / stretchability to the arrangement. Various measures may be taken to ensure electrical safety and to comply with different regulatory frameworks. Direct current (DC) flowing through electrodes or other implanted parts of a system according to any of the aspects of the present disclosure may be a safety concern, as it may cause tissue damage. For example, it has been reported that DC levels as low as 2-3 μA may cause pathological changes in nerve tissue. It is therefore desirable to limit leakage current (DC) to 1 μA or less, such a 0.1 μA or less. This may be achieved by means of a capacitor, also referred to as a DC blocking capacitor, which may be arranged in any of the current pathways. Specifically, the capacitor may be connected in series with two or more electrodes of the implant, such as the ones employed to apply a stimulation signal or a measuring signal. Furthermore, the capacitor may be connected in series with a part of the implant (such as an electrode, an energy source, or a housing) and the body of the patient, thereby reducing any current that might flow between the implant and tissue of the patient. A further advantage of the capacitor relates to prevention of charge accumulation on the electrodes. By coupling a capacitor to the electrodes, the capacitor may help dissipating accumulated charge from the electrodes, thereby allowing them to ‘slide back’ to their operating potential range. The capacitor may be implemented in the circuitry of the medical device, such as the stimulation device discussed above. The capacitor may hence be provided as a component on any of the PCBs 260 or separate from the PCB 260. Denervation is a process of interrupting the nerve supply to a particular organ or area in the body. This can be done for various medical reasons, such as to relieve pain, reduce muscle spasticity, or address certain pathological conditions or illness symptoms. Denervation typically involves cutting off or disrupting the nerve signals to specific part of the body. This can be achieved through various methods, such as surgical removal, the use of chemicals, or by applying thermal or electrical energy to destroy nerve tissue. Surgical denervation may involve physically cutting or removing the nerve or part of it. It is often permanent and may be used in cases where other treatments have failed. Chemical denervation involves injecting a substance (like alcohol or phenol) that destroys or blocks the nerve fibers. This method may often be used for spastic muscles or for pain management. Radiofrequency (RF) ablation employs high-frequency electrical currents to heat up a small area of nerve tissue, thereby blocking further signaling through the nerve. Cryoablation is an example where cold is employed to freeze and destroy the nerve tissue. Denervation can be effective in providing a long term or even permanent effect on the treated tissue. However, it also comes with risks such as undesired side effects and denervation of the ‘wrong’ tissue. Incorrect placement of the ablation tool or administration of the nerve blocking or nerve destructing substance may lead to undesired damages and denervation of tissue not intended to be denervated. Fig.8A shows a system comprising an inhibition device configured to temporarily inhibit a nerve innervating the effector tissue. A sensor 250 may be employed to generate a sensor signal indicative of an effector response in the effector tissue innervated by the nerve, wherein the effector response is at least partly induced by the inhibiting of the nerve. The effector response may be used to determine whether a desired effect is achieved by the inhibition of the nerve before the nerve is being denervated. The present system therefore makes it possible to verify whether the correct nerve is identified before the denervation is performed. This may be verified by determining a response measure based on the sensor signal, wherein the response measure is indicative of the effector response, in order to compare the response measure with a predetermined reference measure, and determining whether the desired effector response has been achieved. The inhibition device may be a stimulation device according to any of the above-discussed examples, comprising one or more signal generating means, such as electrode arrangements 210, 220 or vibration arrangements for delivering an inhibition signal hindering action potentials from passing through the nerve. Fig.8B shows an example of a probe 206 or catheter comprising a first electrode arrangement 210 and a second electrode arrangement 220. The probe 206 is configured to be inserted into the body and arranged such that the first and second electrode arrangements 210, 220 can be placed against the tissue that is to be ablated. In some examples, the probe 206 may be a combined inhibition and denervation device. In other words, the same probe 246 may be used both for temporarily inhibiting the nerve and for ablating it. This can be achieved by operating the electrode arrangements 210, 220 in different modes – an inhibition mode for inhibiting the nerve and a denervation mode for denervating the effector tissue. In the inhibition mode, the electrode arrangements 210, 220 may be operated to apply an inhibition signal as discussed above, whereas in the denervation mode they may be operated to apply an ablation signal for blocking further signaling through the nerve. While the inhibition signal is a relatively weak / low power signal intended not to cause permanent damage to the tissue, the ablation signal may be a relatively strong signal / high power signal. The inhibition signal may typically have a frequency in the range of 1 – 10 kHz, a voltage of about 1 – 15 V, and a current of about 1-50 mA (corresponding to a power of less than 1 W). The ablation signal, on the other hand, may comprise an alternating current in the range of 350 – 500 kHz, a voltage ranging from 500 to 400 V and, in some examples, a power of 50 to 40 W. This may be referred to as a type of radiofrequency ablation (RFA). The inhibition device may in some examples comprise a cooling device configured to cool the nerve to cause a temporary inhibition of the nerve. The cooling device may be formed as a cooling element arranged on the probe 246, which hence may be referred to as a cryoprobe. The cryoprobe 246 may comprise a lumen or channel guiding the cooling gas to the tip of the probe 246, which tip may be placed against the nerve to induce a temporary inhibition. Similar to the electrical probe above, the cryoprobe 246 may be a combined inhibition and ablation device. The difference between the two functions may be determined by the temperature of the probe, more specifically by the degree of cooling of the tissue. A temporary inhibition may occur if the nerve is cooled to a temperature exceeding 0 °C, whereas an ablation (or at least a long-term blocking) may be achieved by freezing the tissue (i.e., lowering the temperature below 0 °C). This allows for the placement of the probe 246 to be verified before the ablation is commenced. In some examples, the inhibition device is operable to deliver a substance to the nerve, such as a toxin temporarily inhibiting the nerve. This may be achieved by means of a toxin administration device 242, of which a particular example is illustrated in Fig.8C. The toxin administration device 242 may comprise a catheter or lumen that can be inserted into the body of the patient and arranged to deliver the substance directly to the relevant nerve. A relatively mild substance may be used to ensure a temporary inhibition. Should a stronger substance be used, a permanent or at least long-term effect may be achieved, and the process may then be referred to as a neurotoxin- induced ablation. By varying the types or concentrations of the administered substance, the toxin administration device 242 may be used both for an initial, temporary inhibition and a more permanent or long-term ablation. Examples of toxins include neurotoxins, such as botulinum toxin and tetanus toxin. It will be appreciated that the denervation device 270 may comprise an ablation device configured to denervate the tissue by means of surgical ablation, RF ablation, cryoablation, laser ablation, heat ablation, electrocautery, and chemical ablation. Fig.8D shows an example of a surgical ablation device 272, comprising a lancet for making incisions in the nerve tissue. The lancet may be understood as a small, sharp instrument that can be used for performing a catheter-based ablation of the nerve. A control unit 240 may be provided for controlling the operation of one or more of the components of the system, i.e., one or more of the inhibition device, the sensor device 250, and the denervation device 270. The control unit 240 may be arranged to receive a sensor signal from the sensor device 250, indicating a physical response in the effector tissue innervated by the stimulated nerve. By detecting a response in the tissue caused by the signal delivered by the inhibition device, it can be assumed that the inhibition device has been inserted into the correct position or part of the patient’s body. Inhibition of a nerve – either temporarily by means of a suppression signal, or permanently by means of ablation – can also be employed to treat sensations of pain, such as phantom pain. Phantom pain is typically a neuropathic pain, relating to the nerves and often being a response to the loss of a limb or body part. Even though the body part is no longer present, nerve endings at the site of the amputation may continue to send pain signals to the brain, making the brain think the body part is still there and experiencing pain. The nerve may also be inhibited to address phantom limb sensation, which is the feeling that an amputated or missing part of the body is still present, but not necessarily painful. Hence, according to some examples, a stimulation device 200 as shown in any of the previous examples may be provided to deliver, directly or indirectly, a suppression signal to a nerve 231, 232 of the patient. Further, the control unit 240 may be configured to control an operation of the stimulation device to suppress or block a propagation of action potentials in an afferent direction of the nerve, thereby reducing the sensation of pain originating from the action potentials. It will be appreciated that the suppression signal, or blocking signal, may be delivered in a similar way and by a similar system as discussed in connection with the unidirectional stimulation disclosed in figure 3A above. However, to block, inhibit, or at least reduce nerve signals generating a sensation of pain, such as phantom pain, or a sensation of a phantom limb, it may suffice to apply the suppression signal. There might not be a need for applying the stimulation signal as well, as the primary objective of the present example is to prevent action potentials from reaching the central nervous system and the brain. Similar to the parameters used for generating the suppression signal for the unidirectional stimulation as discussed above, the control unit 240 may be configured to control an operation of the stimulation device 200 such that the suppression signal varies with a frequency in the range of 1-10 kHz. These frequencies have been observed to reduce the nerve’s capability of transporting action potentials, effectively resulting in a blocking of the nerve. In some examples, a sensor device 250 may be employed for generating a sensor signal indicating any action potentials propagating in the nerve. The sensor device 250 may be similarly configured as any of the sensor devices discussed above in connection with the previous figures and examples, and the sensor signal may hence be used as feedback when controlling the operation of the stimulation signal. The sensor device 250 may, for instance, comprise a sensor electrode configured to be arranged cranial to the suppression electrode. This allows for the suppression signal to be modified in response to the output from the sensor device, and more specifically for the intensity or frequency of the suppression signal to be increased in response to action potentials passing the suppression electrode in the cranial direction. Presence of action potentials cranial to the suppression electrode may indicate that the nerve is still capable of transporting action potentials and that a sufficient blocking is not yet achieved. By adjusting the parameters of the suppression signal accordingly, a more efficient blocking of the nerve may be achieved. Beneficially, the suppression signal is delivered to a nerve via a suppression electrode, such as an electrode similar to the suppression electrodes 221, 222 shown in figure 3A. The location of the suppression electrode may vary depending on the type of pain and from where is originates. However, in general, the suppression signal may be delivered to a sensory nerve, also referred to as an afferent nerve, which is known to play a role in transmitting information from various sensory receptors to the CNS 233. Examples of sensory neurons include mechanoreceptors responding to mechanical stimuly such as pressure, touch, and vibrations; thermoreceptors sensitive to temperature changes; nocireceptors including A-delta fibers transmitting sharp, fast pain and C fibers transmitting dull, slow pain. Further examples include proprioreceptors, providing information about body position, movement, and muscle tension. The suppression signal may be applied to a sensory nerve to block transmission of action potentials from the sensory neurons to the spinal cord and further on to the brain. The suppression electrode 221, 222 may be arranged closer to the sensory receptor / neuron than to the spinal cord so as to ensure a more precise effect (reducing the risk of inadvertent blocking of other signals than the ones responsible for the pain / phantom sensation). In other examples, the suppression electrode 221, 222 may be arranged closer to the spinal cord than to the sensory receptor / neuron, depending on the available space and exact location of the sensory receptor. Figure 9 is a schematic overview of the spinal nerves, and particularly of the sympathetic and parasympathetic nervous system. Figure 9 illustrates the vertebral column 710 and one of the two sympathetic chains 712 (also called sympathetic trunks) located on each side of the vertebral column. Each sympathetic chain 712 comprises a ganglionated nerve trunk. These ganglia are referred to as paravertebral ganglia (25 pairs) and represent one of the sites wherein the sympathetic postganglionic neurons are located. Axons of the sympathetic preganglionic neurons typically synapse on many sympathetic postganglionic neurons in the sympathetic chain. The course of preganglionic and postganglionic sympathetic fibers at different levels of the spinal cord 710 is shown in figure 9. The axons of sympathetic preganglionic neurons located at T1-L3 typically exit the spinal cord 710 via ventral roots, travel a short distance in the corresponding spinal nerves, and then enter the sympathetic chain via the white rami. Typically, the stimulation signal may be applied to the postganglionic part of the sympathetic nerves to address various symptoms, stimulate various effector tissue, and achieve a desired effector response. It will be appreciated that the system according to the present disclosure, which may be used for applying one or more of an activation signal, an inhibition signal, and a suppression signal, may be arranged to deliver such signal(s) to any of the nerves originating from the spinal cord 710 or brainstem 714. In the following, some particular examples of possible stimulation sites and possible effects are discussed. The superior cervical ganglion SCG forms a part of the SNS located in the neck region, near the base of the skull and received preganglionic sympathetic fibers from the thoracic spinal cord (specifically, spinal cord segments T1-T4). These preganglionic fibers synapse with postganglionic neurons in the SCG from where they then continue to their target organs. By applying a stimulation signal – such as an activation signal or an inhibition signal as previously discussed – effector responses such as increase or reduced pupillary dilation, sweating, vasoconstriction, and production can be achieved. Conditions such as Horner’s syndrome, characterized by ptosis (drooping eyelid), miosis (constricted pupil), and anhidrosis (lack of sweating) on one side of the face can be addressed. Further, an effect on cluster headache has been observed. Overall, by stimulating neurons connected to the SCG the autonomic balance and coordination of sympathetic response in the head and neck region can be affected. The sympathetic preganglionic fibers originating from spinal cord segments T1-T4 (or sometimes T5) synapse in the sympathetic trunk ganglia and commonly innervate the respiratory system. For example, the trachea, bronchi, and lungs receive innervation from these spinal cord segments T1-T4. Sympathetic fibers from T1-T4 typically contribute to the regulation of bronchi smooth muscle tone, blood flow, and glandular secretion in the lungs. Sympathetic activation or inhibition caused by application of a stimulation signal to nerve fibers originating from these cord segments may typically affect bronchodilation (for increased / reduced airflow), glandular secretion (increased / reduced mucus production), vasoconstriction (of blood vessels in the lungs), and increased / reduced heart rate (affecting oxygen delivery). Sympathetic fibers from spinal cord segments T5-T12 typically contribute to the innervation of the stomach. These fibers regulate bodily functions such as gastric motility, blood flow, and secretion. However, the vagus nerve (cranial nerve X) is also known to play a significant role in stomach innervation. The liver typically receives sympathetic innervation from spinal cord segments T5-T9. Stimulating these nerves may affect liver blood flow and glucose metabolism. Sympathetic fibers from T5-T9 are known to innervate the pancreas. Stimulation of these nerve may influence pancreatic blood flow and secretion. The adrenal medulla, which forms a part of the adrenal glands, is also known to be innervated by sympathetic fibers from cord segments T5-T12. Stimulating these nerves may result in an increased / reduced release of adrenaline. The small and the large intestine is also innervated by nerves from cord segments T5-T12. Applying a stimulation signal to any of these nerves may affect motility and blood flow, which in turn may affect the digestion, the absorption of nutrients, and fecal consistency. The bladder, gonads, and genitals are typically innervated by sympathetic nerves stemming from the lower end of the spinal cord 710, such as cord segments L1, L2, and L3. Stimulating these nerves may trigger bladder contraction during urination, urinal sphincter contraction, as well as genital sensation, gonadal activity, and motor control. Turning to the parasympathetic nervous system, a major part of the nerves originate from the brainstem, such as the medulla 713 and pons 714. As shown in figure 9, cranial nerve III innervate the ciliary muscle, cranial nerve VII the lacrimal gland, the submandibular gland, and the sublingual gland, and cranial nerve IX the parotid gland. Activating a parasympathetic response in the cranial nerve III may cause the ciliary muscle to relax, whereas an inactivation or inhibition may cause it to contract. Similary, parasympathetic activation of cranial nerves VII and IX may reduce production of tears and / or saliva, whereas a parasympathetic inhibition may increase the tear and / or saliva production. Cranial nerve X is the vagus nerve, which also is discussed below with reference to figure 11. The vagus nerve can be stimulated on a “global” level, before it branches off to various organs in the body, “regionally” to address two or more branches innervating, for example, the digestive system, or “locally” to address specific organs such as the pancreas, kidney, small intestine, or large intestine. The exact location for the application of the stimulation signal may hence be selected based on the desired effector response to be achieved and the part of the body which is to be addressed. As shown in figure 9, branches of cranial nerve X innervate, inter alia, the heart, trachea, bronchi, lung, stomach, liver, pancreas, kidney, small intestine, and large intestine. A parasympathetic activation of these branches typically causes a muscle relaxation or reduced activity inter terms of, for example, glandular secretion. A parasympathetic inhibition, on the other hand, may cause a muscle contraction or increase glandular activity, as this may cause the autonomous tone (i.e., the balance between the PNS and SNS) to shift towards the sympathetic end of the scale. It will therefore be appreciated the stimulation of the PNS may be combined with stimulation of the SNS, as discussed above in connection with figure 1A, to achieve a complementary or synergistic effect adjusting the autonomic tone towards a more parasympathetic dominance or a sympathetic dominance. The sacral nerves originating cord segments S1, S2, S3 are parasympathetic nerves contributing to the sacral plexus. These nerves innervate the lower limb, pelvis, and perineum and may take part in motor and sensory functions of the legs, feet, and pelvic organs. Stimulating these nerves may affect functions such as walking, urination, and sexual activity and may, just as mentioned above, be stimulated in combination with sympathetic complementary nerves originating from cord segments L1, L2, and L3. In some examples, a method for affecting a balance between a sympathetic tone and a parasympathetic tone of the ANS is provided. According to the method, a first stimulation signal may be delivered by a first signal generating means, such as a first stimulation arrangement or first electrode arrangement 210 to a sympathetic nerve of the patient to increase a level of activity of the sympathetic nerve and move the balance towards a sympathetic dominance. The sympathetic nerve may be any of the nerves discussed above with reference to figure 9. Alternatively, a second stimulation signal may be delivered to a parasympathetic nerve to increase a level of activity of the parasympathetic nerve and move the balance towards a parasympathetic dominance. The parasympathetic nerve may be any of the nerves discussed above in connection with figure 9. Hence, the sympathetic and / or parasympathetic nerve may form part of at least one of a cardiovascular system, a respiratory system, a gastrointestinal system, a urinary system, an immune system, a sexual function system, and a stress response system. Adjusting the autonomic tone may affect a heart rate or blood pressure (cardiovascular system), a breathing rate or airway diameter (respiratory system), a sensation of satiety or hunger, or affect peristalsis or digestion (gastrointestinal system), a bladder function (urinary system), an inflammatory response (immune system), erection and ejaculation (sexual function system), and psychological health (a stress response system). The adjustment may be achieved by delivering at least one of the first and second stimulation signals to the respective plexuses, such as the sacral plexus, the cardiac plexus, the celiac plexus, the hypogastric plexus, and the pelvic plexus. In further examples, the stimulation may be delivered to the hypothalamus, or the brainstem (such as pons or medulla). The present concept of nerve stimulation as discussed with reference to figure 9 may be combined with the unidirectional stimulation and the sensor feedback as discussed above in connection with figures 3A-F and 5A-D. For brevity, common features and advantages are therefore not reiterated. Figure 10A is a schematic illustration of a system for treating erectile dysfunction. The system may be similar to the system for sympathetic and parasympathetic stimulation presented in figures 1A-E, and may be combined with the technologies for unidirectional stimulation outlined in figures 3A-F and the feedback mechanisms detailed in figures 5A-F. To maintain brevity, common features and advantages are not repeated in detail here. Erectile dysfunction, often referred to as ‘impotency’, is a common form of sexual dysfunction. The severity of erectile dysfunction can range from mild dysfunction, in which a man is occasionally unable to achieve and sustain an erection sufficient for intercourse, to frequent or moderate dysfunction, to severe or complete dysfunction, in which a man is never able to produce and sustain an erection sufficient for intercourse. The system according to the present disclosure may be employed to address erectile dysfunction over the full range, from mild to complete dysfunction. In a healthy individual, penile erection is generated by increased blood flow into the penis 720 via arterial dilation and decreased blood flow from the penis 720 via venous occlusion. Arterial dilation may be caused by a parasympathetic activation of the smooth muscle cells of the erectile tissue in the penis 720. The cavernous nerve 722 in an example of such a nerve. The activation may include release of a vasodilator and smooth muscle relaxant, such as nitric oxide, which may cause the dilation of arteries such as the cavernous arteries and the helicine arterioles suppling the erectile tissue with blood. The parasympathetic activation may also cause the relaxation of the trabecular network, which is the smooth muscle tissue that surrounds the blood-filled spaces in the erectile tissue. This may lead to increased blood flow and decreased venous outflow in the penis 720, resulting in erection. By applying a stimulation signal to a parasympathetic nerve innervating the erectile tissue, a parasympathetic activation may be triggered, which may result in erection. In the example shown in figure 10A, the stimulation signal may be applied to a branch of the parasympathetic cavernous nerve 722 by means of a stimulation arrangement 220, stimulation generating means, such as an electrode arrangement or vibrator as previously discussed. Is has been observed that penile erection also may be generated by a sympathetic activation of nerves that innervate veins controlling the flow of blood leaving the penis. By applying a stimulation signal to such nerves, such as a branch of the hypogastric nerve plexus 721, a vasoconstrictor and smooth muscle contractant such as norepinephrine may be released. This may cause the constriction of the cavernous veins, which typically are the principal veins that drain the blood from the erectile tissue. The sympathetic activation may also cause the contraction of the deep dorsal vein, which typically is the main vein that drains the blood from the glans penis. These actions reduce the venous outflow from the penis, allowing for an increased intracavernous pressure and maintenance of erection. By applying a stimulation signal to a sympathetic nerve innervating the erectile tissue, a sympathetic activation may be triggered, which may result in erection. In the example shown in figure 10A, the stimulation signal may be applied to a sympathetic branch of the hypogastric nerve plexus 721 by means of a stimulation arrangement 210, such as an electrode arrangement or vibrator as previously described. It will be appreciated that the sympathetic stimulation and the parasympathetic stimulation may be performed individually and separately, or in combination. Combining the two may be particularly beneficial, as the venous vasoconstriction may help increasing the effectiveness of the increased blood supply provided by the arterial vasoconstriction. Hence, in an example, a system for treating erectile dysfunction is provided. The system comprises a stimulation device 200 configured to deliver, directly or indirectly, a first stimulation signal to a sympathetic nerve innervating a penile vein, and a second stimulation signal to a parasympathetic nerve innervating a penile artery. The system further comprises a control unit 240 configured to control an operation of the stimulation device 200 such that the first stimulation signal stimulates an activity of the sympathetic nerve, thereby causing vasoconstriction of the penile vein, and such that the second stimulation signal stimulates an activity of the parasympathetic nerve, thereby causing vasodilation of the penile artery. By increasing the blood flow entering the erectile body and reducing the blood flow exiting the erectile body, engorgement of the erectile body may be induced. The stimulation signals may be delivered in various ways. In some examples, a first stimulation arrangement, such as a first electrode arrangement 210, may be configured to be coupled to the sympathetic nerve at a position between a level of the T11-T2 vertebrae and the pelvic plexus. Further, a second stimulation arrangement, such as a second electrode arrangement 220, may be configured to be coupled to the parasympathetic nerve at a position between a level of sacral spinal cord segments S2-S4 and the pelvic plexus. The control unit 240 may be configured to control the operation of the stimulation device 200 such that at least one of the first stimulation signal and the second stimulation signal is a periodic signal including a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component. As previously mentioned, action potentials may be induced in the nerve by a relatively low frequency signal, such as in the range of 0.1-100 Hz, depending on the type of tissue. In some examples, as sensor device 250 may be provided, which may be configured to generate a sensor signal indicating an effector response caused by the application of the stimulation signal(s). The sensor device 250 may be communicatively coupled with the control unit 240 so as to allow the control unit to use the sensor signal as feedback for controlling the operation of the stimulation device 200 and thus the characteristics of the applied stimulation signals. The sensor device 250 may be arranged to generate a signal indicating one or more of a vasoconstriction of the penile vein, a vasodilation of the penile artery, and an engorgement of the erectile body. Similar to what is disclosed in the examples of figures 5B-D, various types of sensor devices may be employed to measure various physical responses. In some examples, the sensor device may comprise a sensor electrode configured to measure an electric activity and / or electrical impedance in smooth muscle tissue of the penile vein and / or artery. In further examples, the sensor signal may be generated by a strain gauge arranged to measure engorgement of the erectile body. The stimulation signals may be mechanical vibration signals generated by, for example, one or more piezoelectric vibration elements. Alternatively, or additionally, the stimulation signals may be electric signals delivered to the nerves by one or more electrodes. The electrodes may be placed against the nerve, at least partly enclosing the nerve, or inserted into the nerve, as indicated in figures 1B-F. Further, a blocking signal, or suppression signal, may be employed to prevent action potentials, generated by a stimulation signal, from propagating in a certain direction. For example, the blocking signal may be applied caudal to the stimulation signal to reduce the risk of the stimulation signal propagating backwards towards the central nervous system. This may be referred to as unidirectional stimulation and may be achieved by the technology disclosed with reference to the examples of figures 3A-F. Figures 10B-D illustrate the above mechanisms, in which the penile arteries are dilated to increase blood flow to the erectile tissue and the penile veins are constricted to reduce the flow of blood leaving the erectile tissue. Figure 10B is a mid-shaft cross-section of penis, whereas figures 10C and D show portions of the erectile tissue in collapsed and engorged state, respectively. The erectile tissue forms mainly three elongated bodies – two corpora cavernosa 731 and one corpus spongiosum 732. The corpora cavernosa 731 typically run along the length of the penis 751 on the left and right sides, above the corpus spongiosum 732 which runs along the underside of the penis 751, enclosing the urethra and preventing it from punching closed during erection. The blood supply to the erectile tissue 735, such as that of the corpora cavernosum 731, is typically provided by the internal pudendal artery, which branches into the penile arteries 734. Artificial nerve signals generated by the stimulation device 200 trigger the relaxation of smooth muscle cells in the arteries 734 and the erectile tissue 735, leading to the dilation of the arteries 734 and the filling of the erectile tissue 735 with blood. This process is supported by the restriction of venous return by the penile veins 733, such as the tunica albuginea, helping to maintain the erection. The restriction of venous return may be triggered by an artificial stimulation signal delivered by the stimulation device 200. As mentioned above, the arterial dilation may be caused by a parasympathetic activation, whereas the venous constriction may be caused by a sympathetic activation. Figure 10C shows the erectile tissue 735 in a collapsed state and figure 10D shows the erectile tissue when filled with blood. Figure 11 is a schematic illustration of a system for controlling appetite in a patient. The system comprises a stimulation device 200, which may be similarly configured as any of the stimulation devices 200 discussed above. For example, the stimulation device 200 may be similarly configured as the stimulation devices disclosed with reference to figures 1A, 3A, and 5A. The stimulation device 200 may be configured to deliver, directly or indirectly, one or more stimulation signals to the vagus nerve. In particular, the stimulation signal may be delivered to the anterior vagal trunk 752 and / or the posterior vagal trunk 753 of the vagus nerve, as shown in figure 11. The system may further comprise a control unit 240 configured to control an operation of the stimulation device 200. The control unit 240 may operate the stimulation device 200 to deliver a stimulation signal – either electric, or vibrational – controlling or modifying one or more bodily functions regulated at least in part by the vagus nerve. In particular, the stimulation signal may be delivered to affect the patient’s feeling of satiety or hunger. The stimulation signal may be delivered to the vagus nerve by means of a first stimulation arrangement 210, which may be coupled to the anterior gastric division 756 and / or the posterior gastric division 757 of the vagal trunk(s) 752, 753, as indicated in the particular example shown in figure 11. Controlling the patient’s appetite has shown to an effective measure in the treatment of obesity. Obesity is known to be a major risk for many diseases, including cardiovascular disease, diabetes, kidney disease, various types of cancers, as well as musculoskeletal disorders. Traditionally, treatment of obesity imposes a heavy economic burden on the global healthcare system. Common approaches for treating obesity include non-surgical and surgical treatments such as gastric bypass and sleeve gastrectomy. However, there is a high risk of serious complications resulting from invasive procedures, as well as potential of weight rebound or side effects from drugs. Therefore, there is a need for alternative and more effective technologies for affecting and controlling the weight of the human body. Neuromodulation, which typically may be considered a non-destructive and reversible therapeutic strategy, has shown effective in manipulating body functions by stimulating or influencing neurophysiological signals through the neural network to achieve therapeutic purposes. In this context, the vagus nerve (the tenth cranial nerve), may act as a signal bridge to transport information between the brain and various parts of the body. As discussed with reference to figure 9, the vagus nerve originates from the medulla oblongata in the brainstem and travels through the neck, chest, and abdomen, innervating various organs along the way. The vagus nerve is a mixed parasympathetic nerve carrying both sensory and motor information and plays an important role in the function of the digestive system. As shown in the figure 11, the vagus nerve typically comprises two main branches innervating the stomach 751: the anterior vagal trunk 752 and the posterior vagal trunk 753. These typically enter the abdomen through the oesophageal hiatus. Hence, in some examples, the stimulation device 200 may be arranged to deliver the stimulation signal at this position, i.e., at or close to the oesophageal hiatus. The stimulation device 200 may, for instance, be combined with other types of medical devices and implants, such as devices arranged to stretch a portion of the stomach wall to trigger mechanoreceptors to induce a feeling of satiety, or devices invaginated in the stomach fundus to hinder the oesophageal sphincter from moving in relation to the oesophageal hiatus and thereby cause gastroesophageal reflux disease (GERD). In the particular example shown the present figure, however, the stimulation signal may be delivered further down the nerve, after the branch sent to the celiac division 754. More specifically, the first stimulation arrangement 210, such as a first electrode arrangement, may be arranged to contact the gastric division 756, which provides parasympathetic innervation to the smooth muscle and glands of the stomach. Stimulating or inhibiting the gastric division 756 has shown to be effective in affecting gastric motility, secretion, and blood flow, as well as sensory information from the stomach to the brain, such as pain, distension, and acidity levels. In the illustrated example, the first stimulation arrangement 210 delivers the stimulation signal to the anterior gastric division 756. This division typically runs along the lesser curvature of the stomach and innervates effector tissue of the anterior wall of the stomach 751. The first stimulation arrangement 210 may, however, additionally, or alternatively deliver a stimulation signal to the posterior gastric division 757, which typically runs along the lesser curvature of the stomach 751 and innervates effector tissue of the posterior wall of the stomach 751. It will be appreciated that other branches of the gastric divisions 756, 757 may be stimulated in additional or alternative implementations, such as divisions running along the greater curvature of the stomach 751 and innervate the fundus and body of the stomach 751. The stimulation device 200 may be arranged to deliver the stimulation signal to any of or all these branches, depending on the desired effect to be achieved. In further examples, the stimulation device 200 may be arranged to deliver the stimulation signal to other branches and divisions of the anterior or posterior vagal trunks 752, 753, including the hepatic division 758, which innervates the liver and gallbladder, and the pyloric branch 759 which is a branch of the hepatic division 758 and comprises visceral sensory fibers originating in the pyloric canal, pyloric sphincter, and first part of the duodenum. The stimulation signal may be delivered to the pyloric branch 759 to reduce gastric acid secretion and impair the gastric motility, which may have an effect on obesity. The stimulation device 200 may be operated in various modes depending on the desired effect to be achieved, or symptom to be treated. The stimulation device 200 may for example be operated to deliver an inhibition signal for inhibiting activity of the effector tissue innervated by the stimulated nerve. The stimulation device 200 may also be operated to deliver a suppression or blocking signal, preventing action potentials from propagating through the stimulated nerve. Further, the stimulation device 200 may be operated to deliver an activation signal, activating the effector tissue innervated by the stimulated nerve. Various combinations of these operation modes are possible, of which a few will be discussed in the following. In an example, the control unit 240 is configured to control the operation of the stimulation device 200 such that the stimulation signal suppresses the propagation of action potentials in a cranial direction of the vagus nerve. This allows for a hunger signal, conveyed by sensor fibers of the vagus nerve, to be hindered from reaching the patient’s brain. As mentioned above in connection with the unidirectional stimulation, the stimulation signal may be a time-varying signal with an amplitude varying in the range of 1-10kHz. This type of signal, which also may be referred to as an inhibition signal, suppression signal, or blocking signal, may effectively impair the nerve’s ability to transmit action potentials to a degree that reduces the patient’s sensation of hunger. The stimulation signal may typically be applied to nerve fibers that are part of the celiac branches 754 of the vagus nerve. The celiac branches 754 has been observed to detect the stretch and nutrient content of the stomach 751 and intestines, and to send signals to the brain to regulate the appetite or food intake. By blocking the celiac branch 754 of the anterior and / or posterior vagal trunks 752, 753 – or at least reduce the signal transmission – the nerve signals indicating hunger may be prevented from reaching the brain – or at least reduced in signal strength – and the patient may be less hungry. In some examples, the stimulation device 200 may be employed to activate mechanoreceptor cells that detect stomach stretch. Activating these cells may generate a nerve signal indicating that the stomach 751 is full, resulting in a reduced appetite of the patient. Put differently, the stimulation signal may be employed to generate artificial appetite-inhibiting signals to the brain. There have also been observed a type of nerve fibers of the vagus nerve which affect the regulation of blood glucose levels. These nerve fibers are typically part of the celiac branches 754 of the vagus nerve and takes part in the regulation of the production or hormones that control hunger and satiety, such as ghrelin and leptin. By activating or inhibiting such nerve fibers, insulin secretion and glucose metabolism may be modulated, which in turn may have an effect on blood glucose levels and type 2 diabetes. As mentioned above, a nerve blocking effect may be achieved by stimulation signals comprising frequencies in the range of 1-10 kHz. Generating artificial nerve signals, such as action potentials travelling towards the brain to induce a sensation of satiety, may on the other hand require a low-frequency signal as discussed in connection with figure 1A. Examples of such signals include frequencies in the range of 0.1-100 Hz. In some examples, the stimulation signal may be applied to stimulate or suppress a stomach peristalsis. This may, for example, be achieved by inhibiting or stimulating an activity of parasympathetic nerve fibers of the vagus nerve that innervate muscle tissue of the stomach wall. By stimulating a parasympathetic response, for example with frequencies in the range of 0.1-100 Hz, movement of the smooth muscle tissue of the stomach wall (and, in some examples, the intestines), can be suppressed. The stimulation signal may be applied to the celiac division 754, as well as other branches that innervate the intestines, such as the anterior and posterior vagal trunks 752, 753, which has been observed to give off several intestinal nerves. By activating or increasing a parasympathetic response in nerves that help regulate the peristalsis, i.e., the wave-like contraction of the muscles in the stomach 751 and the intestines, the movement of the food along the digestive tract can be slowed down and the stomach be emptied at a slower pace. A similar effect may be achieved by applying a stimulation signal inhibiting a sympathetic response in the muscle tissue of the stomach wall. In some examples, combinations are employed, such that a parasympathetic activity is stimulated while a sympathetic activity is inhibited. A reversed stimulation is also conceivable, in which parasympathetic and / or sympathetic responses in the muscles of the stomach 751 and / or intestines are modulated so as to increase the peristalsis and hence the movement of the food along the digestive tract. Increasing the pace with which the food travels may reduce the time for absorption of nutrients and water, thereby affecting nutritional uptake as well as fecal consistency. In some examples, the peristalsis may be varied over the length of the digestive channel, i.e., over different parts of the small / large intestine. For example, the food may be caused to pass through the small intestine at a relatively high pace to reduce the time for nutritional uptake, and at a slower pace by the end of the large intestine to promote absorption of water and improve fecal consistency. In the particular example illustrated in figure 11, the stimulation device 200 further comprises a second stimulation arrangement 220 for applying a suppression signal suppressing action potentials propagating through the nerve in response to the first stimulation arrangement 210 applying the stimulation signal. The suppression signal, which may be an electric stimulation signal or a vibrational signal, may be employed to achieve a unidirectional stimulation, thereby reducing adverse side effects of the application of the signal. More specifically, the suppression signal may be employed to block action potentials travelling in certain directions, or at least reduce their intensity. Examples of adverse side effects include initiation of undesired or counter-productive feedback to the brain and can result in undesired sensations or activity of the patient. The second stimulation arrangement 220 may be arranged caudal to the first stimulation arrangement 210 to prevent the applied stimulation signal from propagating towards the CNS and the brain. In other examples, the first stimulation arrangement 210 may be arranged caudal to the suppression arrangement 220, as this may prevent the stimulation signal from reaching effector tissue, such as muscle tissue of the stomach wall or sensory receptors. The relative orientation of the first stimulation arrangement 210 and the suppression arrangement 220 may hence vary depending on the specific result to be achieved. Put differently, the location at which the stimulation signal and the suppression signal, respectively, are delivered may be selected depending on where the response to the stimulation signal is to be achieved. The suppression signal may hence be applied at location beyond which the stimulation signal should not pass. In the example shown in figure 11, the suppression signal may be delivered to one or more of the vagal branches or divisions, such as the celiac division 754 or the pyloric branch 759 to reduce the risk of inadvertent stimulation thereof as the stimulation signal is delivered to the gastric division 756. The suppression arrangement 220 may thus be used to block any artificial nerve signals from spreading along nerve fibers which are not intended to be stimulated. The stimulation signal and the suppression signal may be applied at the same time, such as concurrently or simultaneously. In some examples, the suppression signal may be applied with a delay timed to generally match a conduction velocity of the stimulation signal in the vagus nerve. This allows for the suppression signal to be applied for a slightly shorter time compared to a simultaneous application. Reducing the time of the application may reduce the risk for stimulation induced damages to the nervous tissue and fatigue. In the present example, the stimulation signal and the suppression signal are applied by two separate and physically distinct stimulation arrangements 210, 220, such as a respective cuff electrode. However, it will be appreciated that the suppression or blocking capability may be integrated in the same structural arrangement, such as the same cuff electrode, as the stimulation capability. This may be achieved by integrating the means delivering the stimulation signal into the same housing or structural unit as the means delivering the suppression signal. In some examples, the system may comprise a sensor device configured to generate a sensor signal indicating an effector response in the tissue innervated by the nerve to which the stimulation signal is applied. The sensor device may be similarly configured as the devices discussed above in connection with figures 5A-D and similar features and effects are therefore not reiterated here. In some examples, the sensor signal may be indicative of action potentials propagating in the nerve. This information, i.e., the effector response and / or the action potentials, may be used as feedback for controlling the operation of the stimulation device 200. The feedback may, for example, be used to adjust or modify parameters of the stimulation signal. The intensity of the stimulation signal may be increased in response to the sensor signal indicating a too low level of response in the effector tissue or reduced in response to the sensor signal indicating a too high level or response in the effector tissue. Furthermore, the intensity of the suppression signal may be increased in case the sensor response indicates that action potentials are still propagating past the suppression arrangement 220, or reduced in case the sensor response indicate that no action potentials travel past the suppression arrangement 220. Various parameters of the stimulation / suppression signal may be varied depending on the type of result intended to be achieved. The control unit 240 may, for example, use the sensor signal to adjust a frequency of the signal, an amplitude of the signal, or, in case of an electric signal, an electric current of the signal. The sensor signal may be analyzed to retrieve a response measure, which may be indicative of the effector response or a strength of action potentials propagating through the nerve. The response measure may be compared with a reference measure to determine how to adjust one or more parameters of the signal. The reference measure may, for example, be based on one or more previous measurements of the response in the patient, or on previous measurements of responses in other patients. Further, the effector response may be monitored over time so as to detect any drifts or changes over time that may need to be taken into account when controlling the operation of the stimulation device 200. the examples, features and advantages of the system for sympathetic and parasympathetic stimulation presented in figures 1A-E, the unidirectional stimulation outlined in figures 3A-F, and the sensors and feedback mechanisms detailed in figures 5A-F are applicable to the present vagal stimulation system. To maintain brevity, common features and advantages are not repeated here. Figure 12 is a schematic illustration of the alimentary canal 760, or digestive tract, of a typical human body. The walls of the alimentary canal, such as the stomach 751, the small intestine 762 and the large intestine 764, include layers of smooth muscle tissue controlled by the ANS. Alternating contraction and relaxation of these muscles is called peristalsis. Peristaltic waves push the swallowed bolus down the esophagus. In a healthy individual, the swallowed food may typically be treated in the following, exemplary way as described in the following. In the stomach 751, peristalsis churns swallowed food, mixing it with gastric juices. these mechanical and chemical actions further break down food into a substance called chyme. This process, in which foodstuff is turned into chyme, typically takes a few hours. A major part of the nutrient absorption typically occurs in the small intestine 762. When chyme passes from the stomach 751 into the small intestine 762, peristaltic waves shift it back and forth and mix it with digestive enzymes and fluids. The chyme is often pushed for about 3 to 6 hours in the small intestine 762 before it is passed to the large intestine 764 where any final absorption may take place. Peristaltic waves help compact and move waste and indigestible foodstuffs through the large intestine 764 for elimination. The digestive tract 760 is typically endowed with its own, local nervous system, referred to as the enteric nervous system (ENS). An example of the innervation of the digestive tract 760 is shown in figure 12, with the parasympathetic nerves to the left in the figure (including the vagus nerve and the pelvic nerve) and the sympathetic nerves to the right. The ENS has been found to be capable of acting independently of the sympathetic and parasympathetic nervous systems, although it may be influenced by them. The neurons of the ENS typically control the motor functions of the system (i.e., the peristalsis), in addition to the secretion of gastrointestinal enzymes. These neurons communicate through various neurotransmitters similar to the CNS. It has been found that by stimulating the ENS locally, either through application of a stimulation signal to one or more nerves innervating the digestive tract, or through application of a stimulation signal directly to the walls of the stomach 751, the small intestine 762, and / or the large intestine 764, the peristalsis may be controlled or at least affected. The stimulation signal, which may be provided by any of the systems discussed above, such as in connection with figures 1A, 3A, 5A or 11. In some examples, one or more stimulation signals are applied to a parasympathetic nerve (such as the vagus nerve) and / or a sympathetic nerve (e.g., via the prevertebral ganglia). By activating or inhibiting a nervous response in the ENS, the coordination of reflexes controlling the peristalsis and segmentation may be affected of modulated. In an example, a system for affecting a flow of intestinal content in a gastrointestinal tract 760 of a patient is provided. The system comprises a stimulation device 200 configured to deliver a stimulation signal to a plurality of stimulation sites along the gastrointestinal tract 760 to induce an effector response in smooth muscles of a wall of the gastrointestinal tract. The stimulation device may be energized by a source of energy, which may be implanted in the patient or arranged external to the patient, or both. Further, a control unit 240 is provided, which is operably connected to the stimulation device 200 and configured to control an operation of the stimulation device 200 such that the stimulation signal causes at least one of promoting and suppressing peristalsis or segmentation of the gastrointestinal tract. Furthermore, the plurality of stimulation sites may be spaced apart along the gastrointestinal tract 760 by a predetermined spacing. The stimulation signal may be applied in various modes, and to various types of tissue, to depending on the desired effect. In general, the stimulation device 200, delivering the stimulation, may be operated in an activation mode to trigger contraction or relaxation of the smooth muscle tissue, and an inhibition mode inhibiting contraction or relaxation. As discussed above, contraction may typically be triggered by stimulation signals having a relatively low frequency, such as less than 1 Hz, or a few Hz. Examples include 0.1-1 Hz, 1-10 Hz, and 10-100 Hz. Such a stimulation signal may be applied to trigger contraction of the smooth muscles of the walls of the gastrointestinal tract 760. The underlying mechanism is believed to involve parasympathetic activation, which stimulates the ENS to release acetylcholine, a neurotransmitter that binds to muscarinic receptors on the smooth muscle cells and causes them to contract. Additionally, or alternatively, the stimulation signal may be applied to trigger relaxation of the smooth muscles of the walls of the gastrointestinal tract 760. The underlying mechanism is believed to involve sympathetic activation, which stimulates the ENS to release norepinephrine, a neurotransmitter that binds to alpha and beta receptors on the smooth muscle cells and causes them to relax. A stimulation signal may hence be used both for contraction and relaxation, depending on which type of nervous response is triggered. A parasympathetic activation may result in a contraction, while a sympathetic activation may result in a relaxation. By alternating between these types of activations, and / or combining the two, peristalsis and segmentation may be affected. Inhibition or suppression may be applied in a similar manner. Thus, by applying a relatively high frequency signal, such as in a range of 1-10 kHz, the smooth muscle tissue may be inhibited, i.e., contraction or relaxation of the muscle cells may be suppressed. By applying such a stimulation signal to a parasympathetic nerve, contraction of the muscle cells may be suppressed. By applying such a stimulation signal to a sympathetic nerve, relaxation of the muscle cells may be suppressed. Various combinations of inhibition and activation may be applied to achieve the desired effect. In some examples, muscle cells may be activated to contract at the same time as relaxation may be inhibited. This may be alternated with activation of relaxation combined with inhibition of contraction. In other examples, activation signals may be employed in a sequence, in which triggering of contraction cycled with triggering of relaxation. The stimulation signals may be applied at a plurality of locations along the alimentary canal 760. The stimulation signals may be delivered by stimulation arrangements, such as the stimulation arrangements 210, 220 discussed above in connection with figures 1A, 3A, and 5A. The stimulation arrangements 210, 220 may comprise vibration generating means, such as piezoelectric elements, or one or more electrodes for delivering an electric signal, such as a pulsed electric signal. In the following, some examples of application of electric stimulation signals will be discussed. It should however be noted that the discussion applies equally well to other types of stimulation signals, such as vibrations. A plurality of stimulation arrangements, such as electrodes, can be implanted along the alimentary canal 760 to trigger or inhibit a response in the smooth muscles of the walls of the canal 760. Various spacings between the location in which the stimulation signals are delivered are conceivable. The spacing may be selected based on the amount of tissue that can be affected by the applied signal, i.e., the area affected by the stimulation signal. As the response in the muscle tissue may reduce with increasing distance from the application point of the signal, it may be beneficial to place another stimulation arrangement at a position in which the muscular response has decreased below a certain limit. By applying the stimulation signal at regular intervals along at least a part of the alimentary canal 760, the muscular response to the stimulation may be distributed relatively evenly along the canal 760. The spacing between the application points of the signal may also be selected based on a natural wave pattern of the peristalsis. The spacing may for example be selected to correspond with a wavelength of the natural wave pattern caused by the contraction and relaxation of the smooth muscle tissue during segmentation or peristalsis. Beneficially, this may allow the stimulation device 200 to be operated in a way that strengthens or amplifies the natural movement of the walls of the alimentary canal 760, or counteracts the same, depending on the timing or phase of the applied signals. A typical wavelength of the peristalsis, i.e., the distance between two consecutive peaks or throughs of the wave-like muscle contractions that move food along the digestive tract 760, varies with the location and function of the organ involved. For example, in the esophagus, the wavelength is typically about 15 cm and the wave speed about 3 cm / s. In the small intestine 762, the wavelength is about 10 cm and the wave speed about 0.5 cm / s. In the large intestine 764, the wavelength is typically about 20 cm and the wave speed is about 0.2 cm / s. Exemplary spacings of the applications points for the stimulation signal may hence be about 10 cm for the small intestine 762, such as 2-18 cm, such as 6-14 cm, such as 8-12 cm, or multiples thereof. For the large intestine 764, exemplary spacings between the points in which the stimulation signal is applied may include about 20 cm, such as 10-30 cm, such as 14-26 cm, such as 18-22 cm, or multiples thereof. The control unit 240 may be configured to control the application of the stimulation signals based on a natural frequency of the wave pattern of the peristalsis or the segmentation. The stimulation signal may hence be delivered in a pulsed manner, in which a stimulation arrangement is switched between an OFF state and an ON state. In the OFF state, no stimulation signal (or a stimulation signal with a very low, negligible intensity) is delivered to the tissue. In the ON state, the stimulation signal is delivered to induce a response in the tissue. The pacing of the ON and OFF states may be determined based on a frequency of the wave pattern in the smooth muscle tissue. This wave pattern may be the result of a natural movement of the smooth muscle tissue, or a movement induced or controlled by the stimulation device 200. In an example, the stimulation signal may be applied to activate contraction of the muscle tissue when the muscle tissue at application point is about to contract anyway, according to the wave pattern in which the tissue moves. Similarly, the stimulation signal may be applied to cause the muscle tissue to relax at the application point when it is about to contract anyway, according to the wave pattern formed by the contracting and relaxing tissue. In this way, the stimulation signal may be employed to either amplify the movement of the muscle tissue or counteract the movement. With the wavelength and speed examples above, the stimulation signal may be pulsed with a pulse separation or pulse train separation of about 20 s for the small intestine 762, such as 10-30 s, such as 14-26 s, such as 18-22 s. For the large intestine 764, the stimulation signal may be pulsed with pulse separation or pulse train separation of about 100 s, such as 40-160 s, such as 60-140 s, such as 80-120 s. The pulse length, or pulse duration, may be varied based on the strength or intensity of the stimulation signal. Typically, the pulse duration may be in the order of milliseconds, such as the range of 0.01-100 milliseconds, or 100-1000 ms, or in the order of seconds, such as a few seconds. The system allows for the peristalsis to be affected or modulated, which in turn can be used to increase or slow down the pace with which the food moved along the digestive tract. This may be beneficial in various applications and for the treatment of various conditions. Controlling the movement of the food through the digestive tract may, for example, be of interest in connection with stoma, as this allows for a more controlled passage of fecal matter to the stoma. It may also have an effect on obesity, as discussed above, as well as on other types of diseases such as irritable bowel syndrome (IBS). Vasodilation of a blood vessel, or dilation of the blood flow passageway of the blood vessel, is to be understood as an operation increasing a cross-sectional area of the inside space of the vessel. The renal artery is an example of a blood vessel, or luminary organ which can be filled with, and / or convey a flow of, a bodily fluid such as blood. The systems and stimulation devices in the present disclosure may be employed to affect the blood pressure and treat hypotension. In particular, the stimulation of the sympathetic and parasympathetic nervous system discussed above in connection with figures 1A-E, the unidirectional stimulation discussed in connection with figures 3A-F and the feedback mechanisms discussed in connection with figures 5A-D may be employed as outlined below. In the context of the present application, the term “renal artery” may be understood as any blood vessel providing a (main) supply of blood to a kidney. In case of a transplanted or artificial kidney, which often is placed in a location different from the original kidney, such as the iliac fossa, the renal artery may be connected to the external iliac artery. The present inventive concept may thus be applied also to such a blood vessel. Blood pressure is generally referred to as the pressure of circulating blood against the walls of blood vessels. Most of this pressure results from the heart pumping blood through the circulatory system. In common language, the term ‘blood pressure’ often refers to the pressure in the larger arteries. Blood pressure is usually expressed in terms of the systolic pressure (maximum pressure during one heartbeat) over diastolic pressure (minimum pressure between two heartbeats). Blood pressure can be understood as being influenced by cardiac output, systemic vascular resistance and arterial stiffness and may vary depending on situation, emotional state, activity, and relative health / disease states. Blood pressure that is too low is called hypotension, pressure that is consistently too high is called hypertension, and normal pressure is called normotension. Long-term hypertension is a risk factor for many diseases, including stroke, heart disease and kidney failure. The Task force for the management of arterial hypertension of the European Society of Cardiology (ESC) and the European Society of Hypertension (ESH) has provided the following definitions of hypertension: Category Systolic BP, mmHg Diastolic BP, mmHg Optimal < 120 < 80 Normal 120-129 80-84 High normal 130-139 85-89 Grade 1 hypertension 140-159 90-99 Grade 2 hypertension 160-179 100-109 Grade 3 hypertension ≥ 180 ≥ 110 The risk of cardiovascular disease is considered to increase progressively above 115 / 75 mmHg. Below this level there is limited evidence. Vascular resistance is the resistance that must be overcome to push blood through the circulatory system and create flow. The resistance offered by the systemic circulation is known as the systemic vascular resistance (SVR). Vasoconstriction (i.e., decrease in inner blood vessel diameter) increases the SVR, whereas vasodilation (increase in inner diameter) decreases the SVR. Many mechanisms have been proposed to account for the rise in SVR in hypertension. Most evidence implicates either disturbances in the kidneys´ salt and water handling (particularly abnormalities in the intrarenal renin–angiotensin system, RAS) or abnormalities of the sympathetic nervous system. The mechanisms are not mutually exclusive, and it is likely that both contribute to some extent in hypertension. Excessive sodium or insufficient potassium in the diet may lead to excessive intracellular sodium, which may contract vascular smooth muscle tissue, restricting blood flow and so increases the blood pressure. The renin–angiotensin system, RAS, is a hormone system that has been found to regulate blood pressure as well as systemic vascular resistance. When renal blood flow is reduced, which may be the case in for instance hemorrhage or dehydration, juxtaglomerular cells in the kidneys convert the precursor prorenin (already present in the blood) into renin and secrete it directly into circulation. This starts a chain reaction that eventually results in the release of angiotensin II, which has shown to be a potent vasoconstrictive peptide that may cause blood vessels to narrow and the blood pressure to increase accordingly. Angiotensin II is also known to be involved in an increase of extracellular fluid in the body, which also increases blood pressure. The present invention is based on the realization that by causing an electrically induced vasodilation of the renal artery, a reaction that causes a reduction of the systemic vascular resistance may be triggered. The electrically induced vasodilation of the renal artery may be achieved by means of a stimulation device, which may be arranged to stimulate a nerve innervating the renal artery and / or to provide a direct or indirect stimulation of the smooth muscle tissue of the renal artery. The stimulation device may be adapted to alter the vasomotor tone of the smooth muscle cells of the renal artery, causing the cells to relax. Sympathetic stimulation (norepinephrine) has been observed to constrict some blood vessels and dilate others, depending on whether the target cells (i.e., the smooth muscle cells) has alpha- or beta-adrenergic receptors. The sympathetic nervous system can also constrict or dilate vessels just by changing firing frequency. An increased firing frequency may cause the smooth muscle to contract and constrict the vessel, whereas a reduced firing frequency may cause the smooth muscle cells to relax, allowing blood pressure to dilate the vessel. The inventor has realized that the electric stimulation device may be employed to affect the vasomotor tone of the smooth muscle cells to cause the lumen to relax, with the aim of triggering a reduction of the systemic vascular resistance. The electric stimulation device may thus form part of a system for treating a patient with hypertension. While the focus of the present application may be laid on inducing vasodilation to trigger a bodily reaction to reduce the systemic blood pressure, it will be appreciated that the inventive concept of utilizing electrical stimulation for affecting the vasomotor tone of the renal artery may as well be employed for triggering a response increasing the systemic blood pressure. The present inventive concept may hence be applied also for treating patient suffering from hypotension. The aspects, embodiments and examples herein may be combined with implementations wherein electrically induced vasoconstriction is generated by electrical stimulation. The vasoconstriction may be achieved by controlling the electrical stimulation signal such that a contraction of the renal artery is achieved. The inventor has further realized that a control, or regulation, of the electrically induced vasodilation may be achieved by providing a sensor, or sensor device, capable of generating a signal indicative of a blood pressure of the patient. The output signal from the sensor may then be supplied to a control unit, which is configured to control an operation of the stimulation device based on the signal generated by the sensor. The control unit may in some examples utilize the signal from the sensor as a trigger signal, indicating that the stimulation may be initiated and / or ceased. In further examples, the control unit may utilize the signal from the sensor as a feedback control signal, preferably driving the system (and hence the vasodilation or even systemic blood pressure) to a desired state (such as normotension. Exemplary embodiments, effects and advantages of using such an optional sensor is described in further detail in connection with figures 18 and 21A-D. Furthermore, the electrical stimulation signal used for causing the renal artery to relax may inadvertently progress towards the aorta and / or the spinal cord, thereby risking causing unwanted side effects and unpleasant experiences for the patient. Therefore, a signal damping device may according to some implementations of the inventive concept be provided to mitigate the effects of the electrical stimulation signal by damping, disturbing or at least partly cancelling the electrical stimulation signal, thereby limiting the spreading of the electrical stimulation signal to other parts of the patient’s body, as previously discussed. As an introduction to the field in which the present inventive concept can be applied, an exemplary description of the neurophysiology of the renal artery will be described in the following. It is to be noted that the following description of the neurophysiologic mechanisms affecting vasoconstriction of the renal artery is exemplary, simplified where needed, and based on the present knowledge in the art. The purpose of the following exemplary description of the bodily functions and responses is primarily not to limit or define the inventive concept, but to give an exemplary technical / physiological background and context of the inventive concept. Figures 13a and b are schematic illustrations of the kidneys of an adult, human patient. It is common for a normal human to have two kidneys 10, each of which being connected to the circulatory system by means of a renal artery 20 that carries blood from the heart to the kidneys 10 via the aorta 22 and renal vein 30 that drains the kidney 10 and connects it to the inferior vena cava 32. Figure 14 shows the kidneys 10 and the main renal arteries (MRA) 20, which are identified as the renal main blood supply arteries arising from the aorta 22 and ending at its bifurcation split. Although the illustrations in the present application show a single renal artery 20 connecting a respective kidney 10, the inventive concept is equally applicable to patients wherein a kidney is supplied by multiple renal arteries, which may have a separate origin in the aorta 22. In case of multiple renal arteries, the electrical stimulation may be delivered to at least one of the renal arteries, such as the vessel with the greatest diameter (this may consequently be referred to as the MRA). Renal nerves 24 may be identified as fiber structures originating from ganglia in the solar plexus or from the splanchnic nerve collection, forming the renal plexus. The renal nerve plexus may thus be understood as the network of nerve fibers 24 innervating the renal artery 20 as well as the kidney 10. It appears as a major part of the nerves are sympathetic nerves, but the renal plexus may according to some findings also comprise parasympathetic nerves. Beneficially, the stimulation device may be arranged to deliver the electric stimulation to a parasympathetic nerve at least in a branch of a spinal cord dispatching number 10 and along the Coccygeal nerves originating at vertebrae S2-S4, preferably S4. Figures 15a and b illustrate the concept of vasoconstriction and vasodilation. The open cross section of the lumen formed by the blood vessel, such as the renal artery 20 showed in figures 3a and b, may be determined by the vasomotor tone of the smooth muscle cells. The smooth muscle cells of the wall of the renal artery 20 may be innervated by nerve fibers 24, such as for instance sympathetic nerve fibers 24. Sympathetic stimulation has been observed to constrict some blood vessels and dilate others, depending on whether the smooth muscle cells have alpha- or beta-adrenergic receptors. As mentioned above, the sympathetic nervous system can also constrict or dilate vessels just by changing frequency of the action potentials of the nerve fibers 24. In the present figures, an example is illustrated in which an increased action potential frequency (indicated by pulses 26) may cause the smooth muscle tissue to contract, leading to vasoconstriction as illustrated in figure 15a. Reducing the action potential frequency 26 may cause the smooth muscle tissue to relax, leading to vasodilation as illustrated in figure 15b. The stimulation device according to the present inventive concept may be employed to modify the action potential frequency to cause a relaxation of the smooth muscle tissue. Put differently, the stimulation device may be operated to change the vasomotor tone of the smooth muscle tissue of the vessel. The electrical stimulation may be delivered directly to the outer wall of the renal artery 20, or to the nerve fibers 24 innervating the wall of the renal artery 20. Figure 16 shows a renal artery 20 connecting a kidney 10 to the aorta 22, and which may be similar to the renal arteries 20 disclosed in figures 13a-15b. In order to treat hypertension, a stimulation device 110 may be implanted in the patient. The stimulation device 110 may comprise an electrode arrangement, such as a first electrode arrangement 112, configured to deliver an electric stimulation signal to tissue of the patient, thereby causing tissue of a wall portion of the renal artery 20 to relax and dilate a blood flow passageway of the renal artery 20. In the present example, the first electrode arrangement 112 is configured to be attached to the outer wall of the renal artery 20 to deliver an electric stimulation signal to the smooth muscle tissue of the renal artery wall 22. In this way, the smooth muscle tissue may be subject to an electrical stimulation that causes vasodilation. The first electrode arrangement 112 may for example comprise a plurality of electrical electrodes 112a, 112b, each of which having a contacting portion, or electrode element 112a, configured to be arranged to engage the wall of the renal artery 20, and a lead portion 112b electrically connecting the contacting portion 112a to a control unit 114 of the stimulation device 110. The contacting portion 112a of the first electrode arrangement 112 may for example be attached to the wall of the renal artery 20 by means of stitches, for instance allowing for the contacting portion 112a to be at least partly inserted into the tissue on the outer surface of the wall. In further examples, the contacting portion 112a may be arranged on a surface portion, such as a patch (not shown), which in turn may be placed on the tissue of the wall of the renal artery 20. The control unit 114 may be configured to be electrically connected to the electrode arrangement 112 to provide the contacting portions 112a with the electric stimulation signal. The control unit 114 may thus in turn be operatively connected to, or comprise, a power source energizing the control unit 144 and the electrode arrangement 112. Further, the device may according to some embodiments comprise an additional control unit, also referred to as a central control unit, which may be implanted in the body or be a remote unit, arranged outside the body. Further, the control unit 114 may in some examples be configured to transmit control instructions wirelessly to the stimulation device. The number of contact points, in which the electric stimulation signal can be delivered to the smooth muscle tissue, may be selected based on the desired response and the characteristics of the stimulation signal used. Increasing the number of contact points may for example allow for a lower signal amplitude required to generate the desired response (i.e., a relaxation) of the muscle tissue. Conversely, an increase signal amplitude may be used for allowing a reduce in number of contact points. Further, it will be appreciated that some or all of the contacting portions 112a may be individually controlled with respect to the stimulation signal, such that the stimulation signal can be selectively and controllable delivered to one or several of the contact points at the time. The selective application at different contact points may for example be enabled by the control unit 114. When a reduction in systemic vascular resistance is desired, the stimulation device 110 may be operated to generate an electrical stimulation signal that is transmitted from the control unit 114 through the leads 112b to the contacting portions, or electrode elements 112b, which deliver the electrical stimulation signal to the muscle tissue of the wall of the renal artery 20. The electrical stimulation signal may be configured, with respect to e.g. voltage, current or frequency, to trigger a vasodilation response in the renal artery. The vasodilation may in turn result in a systemic response as described above. Figures 17a-h show a renal artery 20 which may be similar to the renal arteries disclosed in the previous figures. Figure 17a-d further disclose a stimulation device which may be similarly configured as the one disclosed in connection with figure 16, and may thus comprise an electrode arrangement 112a, 112b configured to deliver an electric stimulation signal for affecting vasomotor tone in the renal artery 20. The stimulation device may comprise a plurality of contacting portions 112a, or electrode elements 112a, configured to mechanically engage, or be arranged to rest against, tissue of an outer wall of a portion of the renal artery 20 to transmit the electrical stimulation signal to the tissue. In the example in figure 17a, the electrode elements 112a are arranged on an inner surface of a cuff portion 116 configured to be arranged at least partly around the renal artery 20. The cuff portion 116 may in turn be electrically connected to the control unit 114 of the stimulation device 110 by means of a lead 112b. Further configurations are disclosed in figures17b-d, in which the electrode elements 112a are supported by an elongated holder 116 arranged to keep the electrode elements 112a in the desired position at the wall of the renal artery 20. The holder 116, also referred to as a holding device 116, is formed as an elongated device configured to be attached on the outer wall of the renal artery such that a length direction L of the holder 116 extends along a flow direction of the artery 20. Further, an attachment device may be provided to assist in fixating the holder 116 to the renal artery 20. The attachment device may for instance be formed of at least a part of the electrode element 112a, as shown in figure 17c, which may be arranged to at least partly encircle the renal artery 20 and thereby act as a clamp for fixating the holder 116 to the artery 20. Alternatively, or additionally, the attachment device may comprise a suture (not shown) configured to be sutured to the artery to assist in fixating the holder 116. In further examples, such as the configuration shown in figure 17d, the attachment device is configured to be attached to a tissue portion external to the renal artery 20. This may be realized by a supporting rod 116’ or lever adapted to extend from the holder 116 and to be attached to tissue surrounding the renal artery 20 or the kidney 10 by means of, for instance, sutures or staples. Beneficially, the supporting rod 116’ may eventually be embedded or encapsulated by fibrotic tissue assisting keeping the holder 116 and the electrode arrangement 112a in the correct position. It will be appreciated that the holder 116 may be flexible to allow some movement of the stimulation device 110 when implanted. The movement may for instance be caused by the patient moving, or by vasodilation of the artery 20. Further, at least one of a source of energy and control unit of the system may be accommodated in the holder 116. In the above, vasodilation induced by electrical stimulation of nerves have been discussed. Alternative or additional mechanisms for causing the renal artery to expand or contract are however possible, and can beneficially be combined with the inventive concept disclosed in the present application. Two examples of such mechanisms will now be discussed with reference to figures 17e-i, namely thermally induced vasodilation and mechanically induced vasodilation. Figure 17e shows a portion of the renal artery 20 in figures 17a-d, in which a stimulation device 110 having a plurality of heating members 117 have been implanted. In this embodiment, the control unit 114, 124 is configured to control an operation of the stimulation device such that heat is exchanged between the heating members 117 and the wall portion of the renal artery 20 to cause vasodilation thereof. The heat energy may be provided from a source of energy that is implanted inside the renal artery 20, for example integrated in the heating member, or transferred from outside the renal artery 20. In the latter case, the energy may be transferred by means of a wired connection or wirelessly, such as inductively. While the present figure shows heating members 117 shaped as electrodes attached to the interior of the artery, it will be appreciated that they may as well have a tubular shape with an outer surface configured or rest against the inner surface of the artery, or be attached to such a tubular structure to facilitate insertion and possibly attachment in the vessel. An example of such a configuration is disclosed in figure 17f, in which a first and a second catheter 118 are inserted into the artery 20 through the arterial wall and arranged such that the heating members 117 are in thermal contact with the interior side of the artery 20. In yet a further example, the heating member 117 may define a passage through which a blood flow of the renal artery 20 is allowed to pass. The heating member 117 may thus have a shape conforming to a stent abutting the inner surface of the artery. Beneficially, the heating member 117 may comprise a flexible or expandable portion configured to allow the heating member 117 to follow the change in width of the artery 20 such that a width of the passage increases with increased vasodilation and decreases with decreasing vasodilation. The heating member 117 may comprise a shape memory material configured to vary the width of the passage in response to a varying temperature of the heating member. Further, the heating member may comprise a biocompatible material configured to promote fibrotic tissue to promote fibrotic tissue growth thereon – especially on portions arranged outside the artery, such as the external portion of the catheter 118 shown in figure 17f. Preferably, the heating member may be configured to be secured to an inner surface of the artery, where it may be at least partly encapsulated by fibrotic tissue when implanted. Alternatively, or additionally the heating member may be secured to the inner surface by means of sutures or staples. It will be appreciated that the heating member 117 in some examples may have a cooling capacity allowing it to cool the wall of the renal artery 20 to cause the artery to contract. The heating member 117 may thus also be referred to as a thermal member, having the capacity to transfer heat to the wall and / or transfer heat from the wall. The operating mechanism of the thermal member may be based on a resistive heating, or the Peltier effect. In further examples, the heat may be transferred by means of a carrier fluid, such as water, arranged to add or remove heat from the wall of the artery 20. During operation, the control unit 114, 124 may operate the stimulation device 110 such that the thermal member 117 is heated, thereby heating the renal artery 20 locally at position of the thermal member 117. As a result, a dilation of the blood vessel 20 may be achieved, allowing the blood to flow more freely within the renal artery 20 and thereby increase the blood pressure in the kidney 10. Mechanically induced vasodilation will now be discussed with reference to figures 17g-h, in which the renal artery 20 may be expanded by means of dilation device having an expansion member 212 implanted inside the artery. The expansion member 212 is configured to engage at least a portion of a in inner circumferential surface of the renal artery 20 and exert and expanding pressure on the wall of the renal artery 20 to assist in the vasodilation. Thus, the expansion member 212 may be used instead of the thermal or electrical stimulation devices discussed above, or in combination with either of them. Similar to the previous stimulation devices, the operation of the dilation device may be controlled by the control unit 112, 124 and energized by a source of energy similarly configured as the previously discussed sources of energy. Thus, the source of energy may be configured to be implanted inside the renal artery, be integrated in the expansion member, or arranged outside the renal artery. In the latter case the energy may be transferred wirelessly, such as inductively, or by means of a wired connection. Further, the source of energy may be charged by energy wirelessly transferred from outside the renal artery, such as from an extraluminar source of energy which may be implanted elsewhere in the body or arranged outside the body of the patient. The expansion member 212 may be understood as a device suitable for implantation inside the artery and possible to controllably expand and / or contract so as to cause vasodilation. The expansion may for example be caused by means of mechanic, hydraulic or thermal action as will be discussed in the following. Further, the expansion member may comprise a tubular shape having an outer surface configured to rest against the inner surface of the renal artery 20. The expansion member 212 may for instance define a passage through which a blood flow of the renal artery 20 is allowed to pass. The expansion member 212 may be secured at its position by means of sutures or staples, and / or by means of fibrotic tissue at least partly covering or encapsulating the expansion member 212. Preferably, the expansion member 212 comprises a biocompatible material promoting fibrotic tissue growth. In the example shown in figure 17g the expansion member may be a tubular structure, such as a stent-like structure, configured to be fitted within the inner walls of the artery 20. The tubular structure may be formed by a net-like structure, and preferably by a shape- memory materials that varies its shape with the temperature. This allows for the passageway defined by the expansion member to vary its cross-sectional area with the temperature, such that a heating of the tubular structure may cause the structure to expand and thereby induce vasodilation in the renal artery 20. Correspondingly, a cooling of the tubular structure may result in the structure contracting, reducing the pressure on the arterial wall and allowing it to contract again. The heating may for instance be achieved by resistive heating of the shape-memory material, either directly or indirectly, or by means of additional heating elements (such as the ones disclosed in connection with figures 17e-d). An alternative principle of operation of the expansion member 212 is shown in figures 17h-i, in which the expansion member 212 comprises at least one hydraulic expansion means, or bellows 214, operable to cause the expansion member 212 to increase its circumference. In the present example, the expansion member 212 is cylindrical or at least ring-shaped and comprises a first and a second abutment element 213 configured to be arranged to rest against the inner surface of the artery 20. The abutment elements 213 are interconnected by a first and a second bellows 214, which are hydraulically operated via a hydraulic reservoir (not shown) to cause the first and second abutment elements 213 to expand the arterial wall. The hydraulic reservoir may be implanted at a location different from the renal artery, and a motor or pump may be employed to move hydraulic fluid between the bellows and the reservoir to control the expansion and contraction. The motor or pump may be controlled by the control unit 114, 124 as discussed above. Other operation principles are also possible, such as a mechanical expansion means instead of the bellows 214. A threaded, rotating bolt is an example of such a mechanical expansion means, wherein the bolt may be moved into and out from a nut to cause the expansion member 212 to increas...

Claims

CLAIMS 1. A system for treating erectile dysfunction in a male person, comprising: a stimulation device configured to deliver, directly or indirectly: a first stimulation signal to a sympathetic nerve innervating a penile vein of the person; a second stimulation signal to a parasympathetic nerve innervating a penile artery of the person; and a control unit configured to control an operation of the stimulation device such that: the first stimulation signal stimulates an activity of the sympathetic nerve, thereby causing vasoconstriction of the penile vein; and the second stimulation signal stimulates an activity of the parasympathetic nerve, thereby causing vasodilation of the penile artery; wherein the vasodilation of the penile artery increases a blood flow entering an erectile body of the penis and the vasoconstriction of the penile vein reduces a blood flow exiting the erectile body, thereby inducing engorgement of the erectile body.

2. The system according to claim 1, comprising: a first stimulation arrangement configured to deliver the first stimulation signal, the first stimulation arrangement being configured to be coupled to the sympathetic nerve at a position between a level of the T11-L2 vertebrae and the pelvic plexus; and a second stimulation arrangement configured to deliver the second stimulation signal, the second stimulation arrangement being configured to be coupled to the second stimulation signal to the parasympathetic nerve at a position between a level of sacral spinal cord segments S2-S4 and the pelvic plexus.

3. The system according to claim 1 or 2, wherein the control unit is configured to control the operation of the stimulation device such that at least one of the first stimulation signal and the second stimulation signal is a periodic signal including at least one of: a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component.

4. The system according to any of the preceding claims, wherein: each of the first stimulation signal and the second stimulation signal comprises an amplitude varying with a frequency in the range of 0.1-100 Hz.

5. The system according to any of the preceding claims, wherein at least one of the first and second stimulation signals comprises series of pulses having a negative voltage relative to ground.

6. The system according to claim 5, wherein the control unit is configured to operate the stimulation device to generate a positive voltage pulse following one or more negative voltage pulses.

7. The system according to any of the preceding claims, wherein at least one of the first stimulation signal and the second stimulation signal is an electric signal or a vibrational signal.

10. The system according to any of the preceding claims, further comprising: a sensor device configured to generate a sensor signal indicating at least one of vasoconstriction of the penile vein, vasodilation of the penile artery, and engorgement of the erectile body; wherein the control unit is configured to receive the sensor signal and to control an operation of the stimulation device based at least in part on the sensor signal.CLAIMS 1. A system for treating erectile dysfunction in a male person, comprising: a stimulation device configured to deliver, directly or indirectly: a first stimulation signal to a sympathetic nerve innervating a penile vein of the person; a second stimulation signal to a parasympathetic nerve innervating a penile artery of the person; and a control unit configured to control an operation of the stimulation device such that: the first stimulation signal stimulates an activity of the sympathetic nerve, thereby causing vasoconstriction of the penile vein; and the second stimulation signal stimulates an activity of the parasympathetic nerve, thereby causing vasodilation of the penile artery; wherein the vasodilation of the penile artery increases a blood flow entering an erectile body of the penis and the vasoconstriction of the penile vein reduces a blood flow exiting the erectile body, thereby inducing engorgement of the erectile body.

2. The system according to claim 1, comprising: a first stimulation arrangement configured to deliver the first stimulation signal, the first stimulation arrangement being configured to be coupled to the sympathetic nerve at a position between a level of the T11-L2 vertebrae and the pelvic plexus; and a second stimulation arrangement configured to deliver the second stimulation signal, the second stimulation arrangement being configured to be coupled to the second stimulation signal to the parasympathetic nerve at a position between a level of sacral spinal cord segments S2-S4 and the pelvic plexus.

3. The system according to claim 1 or 2, wherein the control unit is configured to control the operation of the stimulation device such that at least one of the first stimulation signal and the second stimulation signal is a periodic signal including at least one of: a variable frequency component, a variable duty cycle component, a variable amplitude component, and a variable pause component.

4. The system according to any of the preceding claims, wherein: each of the first stimulation signal and the second stimulation signal comprises an amplitude varying with a frequency in the range of 0.1-100 Hz.

5. The system according to any of the preceding claims, wherein at least one of the first and second stimulation signals comprises series of pulses having a negative voltage relative to ground.

6. The system according to claim 5, wherein the control unit is configured to operate the stimulation device to generate a positive voltage pulse following one or more negative voltage pulses.

7. The system according to any of the preceding claims, wherein at least one of the first stimulation signal and the second stimulation signal is an electric signal or a vibrational signal.

10. The system according to any of the preceding claims, further comprising: a sensor device configured to generate a sensor signal indicating at least one of vasoconstriction of the penile vein, vasodilation of the penile artery, and engorgement of the erectile body;wherein the control unit is configured to receive the sensor signal and to control an operation of the stimulation device based at least in part on the sensor signal.

11. The system according to claim 10, wherein the sensor device comprises a sensor electrode configured to measure an electric activity in smooth muscle tissue of the penile vein and / or the penile artery.

12. The system according to claim 10, wherein the device comprises a sensor electrode configured to measure a change in electrical impedance in smooth muscle tissue of the penile vein and / or the penile artery.

13. The system according to claim 11 or 12, wherein: the sensor electrode is configured to be arranged at the penile vein and / or the penile artery; the sensor further comprises a reference electrode, and the sensor device is configured to generate the sensor signal based on an electrical interaction between the sensor electrode and the reference electrode.

14. The system according to claim 13, wherein the reference electrode is formed by a housing of the stimulation device or the sensor device.

15. The system according to claim 10, wherein the sensor signal is generated by a strain gauge and wherein the sensor signal indicates an engorgement of the erectile body.

16. The system according to any of claims 10-15, wherein the control unit is configured to determine a response measure based on the sensor signal, the response measure being indicative of said at least one of vasoconstriction of the penile vein, vasodilation of the penile artery, and engorgement of the erectile body.

17. The system according to claim 16, wherein the control unit is configured to: compare the response measure with a predetermined reference measure; and in response to the response measure being below the reference measure, increase an intensity of the first stimulation signal to stimulate the activity in the in the sympathetic nerve and / or increase an intensity of the second stimulation signal to increase the activity of the parasympathetic nerve, and in response to the response measure exceeding the reference measure, reduce the intensity of the first stimulation signal to inhibit the activity of the sympathetic nerve and / or reduce the intensity of the second stimulation signal to inhibit the activity of the parasympathetic nerve.

18. The method according to claim 17, wherein the predetermined reference measure is based on a previous measurement on the person.

19. The method according to claim 17 or 18, wherein the predetermined reference measure is based on previous measurement on other persons.

20. The system according to any of the preceding claims, wherein the stimulation device comprises a first stimulation arrangement configured to deliver the first stimulation signal and a second stimulation arrangement configured to deliver the second stimulation signal.

21. The system according to claim 20, wherein the first stimulation arrangement comprises a first stimulation electrode and a second stimulation electrode, the first stimulation electrode and the second stimulation electrode are configured to be spaced apart along the sympathetic nerve innervating the penile vein of the person.

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