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Bernard Cohen - One of the best experts on this subject based on the ideXlab platform.
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Vasovagal Oscillations and Vasovagal Responses Produced by the Vestibulo-Sympathetic Reflex in the Rat
Frontiers in Neurology, 2014Co-Authors: Sergei B. Yakushin, Giovanni Martinelli, Theodore Raphan, Yongqing Xiang, Bernard CohenAbstract:Sinusoidal galvanic vestibular stimulation (sGVS) induces oscillations in blood pressure (BP) and heart rate (HR) i.e., vasovagal oscillations, and decreases in BP and HR i.e., vasovagal responses, in isoflurane-anesthetized rats. We determined the characteristics of the vasovagal oscillations, assessed their role in the generation of vasovagal responses and determined whether they could be induced by monaural as well as by binaural sGVS and by oscillation in pitch. Wavelet analyses were used to determine the power distributions of the waveforms. Monaural and binaural sGVS and pitch generated vasovagal oscillations at the frequency and at twice the frequency of stimulation. Vasovagal oscillations and vasovagal responses were maximally induced at low stimulus frequencies (0.025-0.05 Hz). The oscillations were attenuated and the responses were rarely induced at higher stimulus frequencies. Vasovagal oscillations could occur without induction of vasovagal responses, but vasovagal responses were always associated with a vasovagal oscillation. We posit that the vasovagal oscillations originate in a low frequency band that, when appropriately activated by strong Sympathetic stimulation, can generate vasovagal oscillations as a precursor for vasovagal responses and syncope. We further suggest that the activity responsible for the vasovagal oscillations arises in low frequency, otolith neurons with orientation vectors close to the vertical axis of the head. These neurons are likely to provide critical input to the Vestibulo-Sympathetic Reflex to increase BP and HR upon changes in head position relative to gravity, and to contribute to the production of vasovagal oscillations and vasovagal responses and syncope when the baroReflex is inactivated.
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electrical activation of the human vestibulo Sympathetic Reflex
Experimental Brain Research, 2006Co-Authors: Andrei Voustianiouk, Horacio Kaufmann, Andre Diedrich, Theodore Raphan, Italo Biaggioni, Hamish G Macdougall, Dmitri Ogorodnikov, Bernard CohenAbstract:Muscle Sympathetic nerve activity (MSNA) is modulated on a beat-to-beat basis by the baroReflex. Vestibular input from the otolith organs also modulates MSNA, but characteristics of the vestibulo-Sympathetic Reflex (VSR) are largely unknown. The purpose of this study was to elicit the VSR with electrical stimulation to estimate its latency in generating MSNA. The vestibular nerves of seven subjects were stimulated across the mastoids with short trains of high frequency, constant current pulses. Pulse trains were delivered every fourth heartbeat at delays of 300–700 ms after the R wave of the electrocardiogram. Vestibular nerve stimulation given 500 ms after the R wave significantly increased baroReflex-driven MSNA, as well as the diastolic blood pressure threshold at which bursts of MSNA occurred. These changes were specific to beats in which vestibular stimulation was applied. Electrical stimulation across the shoulders provided a control condition. When trans-shoulder trials were subtracted from trials with vestibular nerve stimulation, eliminating the background baroReflex-driven Sympathetic activity, there was a sharp increase in MSNA beginning 660 ms after the vestibular nerve stimulus and lasting for about 60 ms. The increase in the MSNA produced by vestibular nerve stimulation, and the associated increase in the diastolic blood pressure threshold at which the baroReflex-driven bursts occurred, provide evidence for the presence of a short-latency VSR in humans that is likely to be important for the maintenance of blood pressure during rapid changes in head and body position with respect to gravity.
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vestibular control of Sympathetic activity an otolith Sympathetic Reflex in humans
Experimental Brain Research, 2002Co-Authors: Horacio Kaufmann, Andrei Voustianiouk, Andre Diedrich, Theodore Raphan, Italo Biaggioni, Fernando Costa, R Clarke, Martin Gizzi, Bernard CohenAbstract:It has been proposed that a vestibular Reflex originating in the otolith organs and other body graviceptors modulates Sympathetic activity during changes in posture with regard to gravity. To test this hypothesis, we selectively stimulated otolith and body graviceptors sinusoidally along different head axes in the coronal plane with off-vertical axis rotation (OVAR) and recorded Sympathetic efferent activity in the peroneal nerve (muscle Sympathetic nerve activity, MSNA), blood pressure, heart rate, and respiratory rate. All parameters were entrained during OVAR at the frequency of rotation, with MSNA increasing in nose-up positions during forward linear acceleration and decreasing when nose-down. MSNA was correlated closely with blood pressure when subjects were within ±90° of nose-down positions with a delay of 1.4 s, the normal latency of baroReflex-driven changes in MSNA. Thus, in the nose-down position, MSNA was probably driven by baroReflex afferents. In contrast, when subjects were within ±45° of the nose-up position, i.e., when positive linear acceleration was maximal along the naso-ocipital axis, MSNA was closely related to gravitational acceleration at a latency of 0.4 s. This delay is too short for MSNA changes to be mediated by the baroReflex, but it is compatible with the delay of a response originating in the vestibular system. We postulate that a vestibuloSympathetic Reflex, probably originating mainly in the otolith organs, contributes to blood pressure maintenance during forward linear acceleration. Because of its short latency, this Reflex may be one of the earliest mechanisms to sustain blood pressure upon standing.
Hermann O. Handwerker - One of the best experts on this subject based on the ideXlab platform.
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Sympathetic vasoconstrictor Reflex pattern in patients with complex regional pain syndrome
Pain, 1998Co-Authors: Frank Birklein, B. Riedl, B Neundorfer, Hermann O. HandwerkerAbstract:Twenty patients suffering from complex regional pain syndrome (CRPS) and 21 healthy control subjects were examined to evaluate Sympathetic Reflex vasoconstriction. The mean age of the 12 female and eight male patients was 48.9 (21-72) years. At the time of investigation the median duration of the disease was 8.5 weeks (2-70). Twenty-one healthy subjects were investigated for control. Different maneuvers, such as the veno-arteriolar Reflex (VAR), inspiratory gasp (IG), cold pressor test (CP) and mental arithmetic (MA), were employed to induce vasoconstriction while the cutaneous blood flow of the affected and the contralateral limb was recorded. In addition, the skin temperature of both limbs was measured by infrared thermography. In 14 of 20 patients and in 14 of 21 control subjects vasoconstriction due to the provocation tests could be measured, while the remaining six patients and seven controls showed vasodilatation in at least one test, and by that they were excluded from analysis of vasoconstrictor Reflex pattern. After thermoregulatory adaptation skin temperature was not different between the affected and the unaffected limb. Sympathetic Reflex vasoconstriction triggered by MA which represents cortical generated, moderate vasoconstrictor stimulus, was significantly reduced on the affected limb (102.9% of prestimulus period) when compared to the control limb (85.0%, P < 0.002) or to controls (84.8%, P < 0.001). VAR (pure postganglionic), IG and CP (both spinal and supraspinal), representing stronger vasoconstrictor stimuli, revealed no significant side to side difference of Sympathetic vasoconstriction and no significant difference as compared to controls. In conclusion our findings prove impairment of Sympathetic vasoconstrictor activity after central vasoconstrictor stimulation in CRPS, and possible mechanisms are discussed.
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Effects of cutaneous histamine application in patients with Sympathetic Reflex dystrophy.
Muscle & Nerve, 1997Co-Authors: F Birklein, D Claus, B Neundorfer, B. Riedl, Hermann O. HandwerkerAbstract:Thirty-six patients suffering from acute Reflex Sympathetic dystrophy (RSD) were examined in order to evaluate nociceptive C-fibers. Axon Reflex vasodilatation was induced by iontophoresis of histamine and recorded (laser Doppler flux). The strength of concomitant sensation was rated on a visual analogue scale, and the quality was characterized as itching or burning pain. Skin temperature was recorded by infrared thermography. The results were compared with investigations of unaffected limbs of patients and volunteers. The histamine-induced sensation on the symptomatic side was more often burning pain than itching (P < 0.001), and skin temperature was increased on the affected limb (P < 0.001). Axon Reflex vasodilatation and the strength of sensations were unaltered. In conclusion, this study rules out a significant deterioration of afferent C-fibers in RSD, but gives evidence of sensitization of nociceptive function. This nociceptive sensitization has to be taken into consideration for effective treatment of RSD. © 1997 John Wiley & Sons, Inc. Muscle Nerve20: 1389–1395, 1997
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Sudomotor function in Sympathetic Reflex dystrophy
Pain, 1997Co-Authors: F Birklein, R Sittl, A Spitzer, D Claus, B Neundorfer, Hermann O. HandwerkerAbstract:Sudomotor functions were studied in 27 patients suffering from Reflex Sympathetic dystrophy (RSD) according to the criteria established by Bonica (18 women, 9 men; mean age 50±12.3 years; median duration of disease 8 weeks, range 2–468 weeks). To measure local sweating rates, two small chambers (5 cm2) were affixed to corresponding areas of hairy skin on the affected and unaffected limbs. Dry nitrogen gas was passed through the chambers (270 ml/min) and evaporation was recorded at both devices with hygrometers. Thermoregulatory sweating (TST) was induced by raising body temperature (intake of 0.5 l hot tea and infra-red irradiation). Local sweating was also induced through an axon Reflex (QSART) by transcutaneous iontophoretic application of carbachol (5 min, 1 mA). In addition, skin temperature was measured on the affected and unaffected side by infra-red thermography. Mean skin temperature was significantly higher on the affected side (P
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sudomotor function in Sympathetic Reflex dystrophy
Pain, 1997Co-Authors: F Birklein, R Sittl, A Spitzer, D Claus, B Neundorfer, Hermann O. HandwerkerAbstract:Sudomotor functions were studied in 27 patients suffering from Reflex Sympathetic dystrophy (RSD) according to the criteria established by Bonica (18 women, 9 men; mean age 50±12.3 years; median duration of disease 8 weeks, range 2–468 weeks). To measure local sweating rates, two small chambers (5 cm2) were affixed to corresponding areas of hairy skin on the affected and unaffected limbs. Dry nitrogen gas was passed through the chambers (270 ml/min) and evaporation was recorded at both devices with hygrometers. Thermoregulatory sweating (TST) was induced by raising body temperature (intake of 0.5 l hot tea and infra-red irradiation). Local sweating was also induced through an axon Reflex (QSART) by transcutaneous iontophoretic application of carbachol (5 min, 1 mA). In addition, skin temperature was measured on the affected and unaffected side by infra-red thermography. Mean skin temperature was significantly higher on the affected side (P<0.003). In spite of the temperature differences, there was no difference in basal sweating on the affected and unaffected side. However, both methods of sudomotor stimulation lead to significantly greater sweating responses on the affected compared to the unaffected side (TST: P<0.05, QSART: P<0.004). Latency to onset of sweating was significantly shorter on the affected side under both test conditions (P<0.04 and P<0.003, respectively). Sweat responses were not correlated to absolute skin temperature but were probably related to the increased blood flow on the affected side. Our findings imply a differential disturbance of vasomotor and sudomotor mechanisms in affected skin. Whereas vasoconstrictor activity is apparently lowered, sudomotor output is either unaltered or may even be enhanced.
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Asymmetry and time-course of cutaneous Sympathetic Reflex responses following sustained excitation of chemosensitive nociceptors in humans
Journal of The Autonomic Nervous System, 1996Co-Authors: Walter Magerl, Martin Koltzenburg, Jörg M. Schmitz, Hermann O. HandwerkerAbstract:Abstract Sympathetic Reflex responses were elicited in human volunteers by sustained selective excitation of nociceptors by noxious chemicals, namely topical application of mustard oil which elicited burning pain, or histamine which induced itching in a skin area of 5 cm 2 on the volar aspect of one forearm. Stimulus-related Sympathetic Reflex responses were studied by means of computer-assisted infrared thermography of the palmar aspects of both hands. Nociceptive stimulation induced a decrease of skin surface temperature in both hands interpreted as vasoconstriction. The magnitude of the Reflex cooling was correlated with the magnitude of the sensation ( r = 0.49), but independent of the quality of sensation (itch or pain). The temperature reduction was maintained for more than 30 min and its time-course matched the time-courses of pain or itch sensations. It is concluded that the sustained and selective excitation of nociceptors elicits a sustained Sympathetic Reflex response, which adapts very slowly. The time-course of the Reflexes suggests that these are not arousal responses, but may be indicators of nociceptive processing in conscious humans. Contralateral temperature decreases were consistently smaller than ipsilateral ones. Thus, sustained nociceptive-specific vasoconstrictor Reflexes may be somatotopically organised with an emphasis on areas close to the painful stimulus (homotopic), which has so far only been shown in animals. The study thus demonstrates for the first time in humans the presence of a Sympathetic Reflex asymmetry, which is specific for nociceptive afferent input.
Giovanni Martinelli - One of the best experts on this subject based on the ideXlab platform.
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projection neurons of the vestibulo Sympathetic Reflex pathway
The Journal of Comparative Neurology, 2014Co-Authors: Victor L Friedrich, Giovanni MartinelliAbstract:Changes in head position and posture are detected by the vestibular system and are normally followed by rapid modifications in blood pressure. These compensatory adjustments, which allow humans to stand up without fainting, are mediated by integration of vestibular system pathways with blood pressure control centers in the ventrolateral medulla. Orthostatic hypotension can reflect altered activity of this neural circuitry. Vestibular sensory input to the vestibulo-Sympathetic pathway terminates on cells in the vestibular nuclear complex, which in turn project to brainstem sites involved in the regulation of cardiovascular activity, including the rostral and caudal ventrolateral medullary regions (RVLM and CVLM, respectively). In the present study, sinusoidal galvanic vestibular stimulation was used to activate this pathway, and activated neurons were identified through detection of c-Fos protein. The retrograde tracer FluoroGold was injected into the RVLM or CVLM of these animals, and immunofluorescence studies of vestibular neurons were conducted to visualize c-Fos protein and FluoroGold concomitantly. We observed activated projection neurons of the vestibulo-Sympathetic Reflex pathway in the caudal half of the spinal, medial and parvocellular medial vestibular nuclei. Approximately two-thirds of the cells were ipsilateral to FluoroGold injection sites in both RVLM and CVLM and the remainders were contralateral. As a group, cells projecting to RVLM were located slightly rostral to those with terminals in CVLM. Individual activated projection neurons were multipolar, globular or fusiform in shape. This study provides the first direct demonstration of the central vestibular neurons that mediate the vestibulo-Sympathetic Reflex.
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Vasovagal Oscillations and Vasovagal Responses Produced by the Vestibulo-Sympathetic Reflex in the Rat
Frontiers in Neurology, 2014Co-Authors: Sergei B. Yakushin, Giovanni Martinelli, Theodore Raphan, Yongqing Xiang, Bernard CohenAbstract:Sinusoidal galvanic vestibular stimulation (sGVS) induces oscillations in blood pressure (BP) and heart rate (HR) i.e., vasovagal oscillations, and decreases in BP and HR i.e., vasovagal responses, in isoflurane-anesthetized rats. We determined the characteristics of the vasovagal oscillations, assessed their role in the generation of vasovagal responses and determined whether they could be induced by monaural as well as by binaural sGVS and by oscillation in pitch. Wavelet analyses were used to determine the power distributions of the waveforms. Monaural and binaural sGVS and pitch generated vasovagal oscillations at the frequency and at twice the frequency of stimulation. Vasovagal oscillations and vasovagal responses were maximally induced at low stimulus frequencies (0.025-0.05 Hz). The oscillations were attenuated and the responses were rarely induced at higher stimulus frequencies. Vasovagal oscillations could occur without induction of vasovagal responses, but vasovagal responses were always associated with a vasovagal oscillation. We posit that the vasovagal oscillations originate in a low frequency band that, when appropriately activated by strong Sympathetic stimulation, can generate vasovagal oscillations as a precursor for vasovagal responses and syncope. We further suggest that the activity responsible for the vasovagal oscillations arises in low frequency, otolith neurons with orientation vectors close to the vertical axis of the head. These neurons are likely to provide critical input to the Vestibulo-Sympathetic Reflex to increase BP and HR upon changes in head position relative to gravity, and to contribute to the production of vasovagal oscillations and vasovagal responses and syncope when the baroReflex is inactivated.
Theodore Raphan - One of the best experts on this subject based on the ideXlab platform.
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Vasovagal Oscillations and Vasovagal Responses Produced by the Vestibulo-Sympathetic Reflex in the Rat
Frontiers in Neurology, 2014Co-Authors: Sergei B. Yakushin, Giovanni Martinelli, Theodore Raphan, Yongqing Xiang, Bernard CohenAbstract:Sinusoidal galvanic vestibular stimulation (sGVS) induces oscillations in blood pressure (BP) and heart rate (HR) i.e., vasovagal oscillations, and decreases in BP and HR i.e., vasovagal responses, in isoflurane-anesthetized rats. We determined the characteristics of the vasovagal oscillations, assessed their role in the generation of vasovagal responses and determined whether they could be induced by monaural as well as by binaural sGVS and by oscillation in pitch. Wavelet analyses were used to determine the power distributions of the waveforms. Monaural and binaural sGVS and pitch generated vasovagal oscillations at the frequency and at twice the frequency of stimulation. Vasovagal oscillations and vasovagal responses were maximally induced at low stimulus frequencies (0.025-0.05 Hz). The oscillations were attenuated and the responses were rarely induced at higher stimulus frequencies. Vasovagal oscillations could occur without induction of vasovagal responses, but vasovagal responses were always associated with a vasovagal oscillation. We posit that the vasovagal oscillations originate in a low frequency band that, when appropriately activated by strong Sympathetic stimulation, can generate vasovagal oscillations as a precursor for vasovagal responses and syncope. We further suggest that the activity responsible for the vasovagal oscillations arises in low frequency, otolith neurons with orientation vectors close to the vertical axis of the head. These neurons are likely to provide critical input to the Vestibulo-Sympathetic Reflex to increase BP and HR upon changes in head position relative to gravity, and to contribute to the production of vasovagal oscillations and vasovagal responses and syncope when the baroReflex is inactivated.
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electrical activation of the human vestibulo Sympathetic Reflex
Experimental Brain Research, 2006Co-Authors: Andrei Voustianiouk, Horacio Kaufmann, Andre Diedrich, Theodore Raphan, Italo Biaggioni, Hamish G Macdougall, Dmitri Ogorodnikov, Bernard CohenAbstract:Muscle Sympathetic nerve activity (MSNA) is modulated on a beat-to-beat basis by the baroReflex. Vestibular input from the otolith organs also modulates MSNA, but characteristics of the vestibulo-Sympathetic Reflex (VSR) are largely unknown. The purpose of this study was to elicit the VSR with electrical stimulation to estimate its latency in generating MSNA. The vestibular nerves of seven subjects were stimulated across the mastoids with short trains of high frequency, constant current pulses. Pulse trains were delivered every fourth heartbeat at delays of 300–700 ms after the R wave of the electrocardiogram. Vestibular nerve stimulation given 500 ms after the R wave significantly increased baroReflex-driven MSNA, as well as the diastolic blood pressure threshold at which bursts of MSNA occurred. These changes were specific to beats in which vestibular stimulation was applied. Electrical stimulation across the shoulders provided a control condition. When trans-shoulder trials were subtracted from trials with vestibular nerve stimulation, eliminating the background baroReflex-driven Sympathetic activity, there was a sharp increase in MSNA beginning 660 ms after the vestibular nerve stimulus and lasting for about 60 ms. The increase in the MSNA produced by vestibular nerve stimulation, and the associated increase in the diastolic blood pressure threshold at which the baroReflex-driven bursts occurred, provide evidence for the presence of a short-latency VSR in humans that is likely to be important for the maintenance of blood pressure during rapid changes in head and body position with respect to gravity.
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vestibular control of Sympathetic activity an otolith Sympathetic Reflex in humans
Experimental Brain Research, 2002Co-Authors: Horacio Kaufmann, Andrei Voustianiouk, Andre Diedrich, Theodore Raphan, Italo Biaggioni, Fernando Costa, R Clarke, Martin Gizzi, Bernard CohenAbstract:It has been proposed that a vestibular Reflex originating in the otolith organs and other body graviceptors modulates Sympathetic activity during changes in posture with regard to gravity. To test this hypothesis, we selectively stimulated otolith and body graviceptors sinusoidally along different head axes in the coronal plane with off-vertical axis rotation (OVAR) and recorded Sympathetic efferent activity in the peroneal nerve (muscle Sympathetic nerve activity, MSNA), blood pressure, heart rate, and respiratory rate. All parameters were entrained during OVAR at the frequency of rotation, with MSNA increasing in nose-up positions during forward linear acceleration and decreasing when nose-down. MSNA was correlated closely with blood pressure when subjects were within ±90° of nose-down positions with a delay of 1.4 s, the normal latency of baroReflex-driven changes in MSNA. Thus, in the nose-down position, MSNA was probably driven by baroReflex afferents. In contrast, when subjects were within ±45° of the nose-up position, i.e., when positive linear acceleration was maximal along the naso-ocipital axis, MSNA was closely related to gravitational acceleration at a latency of 0.4 s. This delay is too short for MSNA changes to be mediated by the baroReflex, but it is compatible with the delay of a response originating in the vestibular system. We postulate that a vestibuloSympathetic Reflex, probably originating mainly in the otolith organs, contributes to blood pressure maintenance during forward linear acceleration. Because of its short latency, this Reflex may be one of the earliest mechanisms to sustain blood pressure upon standing.
I Z Shahid - One of the best experts on this subject based on the ideXlab platform.
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orexin a in rat rostral ventrolateral medulla is pressor sympatho excitatory increases barosensitivity and attenuates the somato Sympathetic Reflex
British Journal of Pharmacology, 2012Co-Authors: Ahmed A Rahman, I Z Shahid, Paul M. PilowskyAbstract:BACKGROUND AND PURPOSE The rostral ventrolateral medulla (RVLM) maintains Sympathetic nerve activity (SNA), and integrates adaptive Reflexes. Orexin A-immunoreactive neurones in the lateral hypothalamus project to the RVLM. Microinjection of orexin A into RVLM increases blood pressure and heart rate. However, the expression of orexin receptors, and effects of orexin A in the RVLM on splanchnic SNA (sSNA), respiration and adaptive Reflexes are unknown. EXPERIMENTAL APPROACH The effect of orexin A on baseline cardio-respiratory variables as well as the somato-Sympathetic, baroreceptor and chemoreceptor Reflexes in RVLM were investigated in urethane-anaesthetized, vagotomized and artificially ventilated male Sprague-Dawley rats (n= 50). orexin A and its receptors were detected with fluorescence immunohistochemistry. KEY RESULTS Tyrosine hydroxylase-immunoreactive neurones in the RVLM were frequently co-localized with orexin 1 (OX1) and orexin 2 (OX2) receptors and closely apposed to orexin A-immunoreactive terminals. Orexin A injected into the RVLM was pressor and sympatho-excitatory. Peak effects were observed at 50 pmol with increased mean arterial pressure (42 mmHg) and SNA (45%). Responses to orexin A (50 pmol) were attenuated by the OX1 receptor antagonist, SB334867, and reproduced by the OX2 receptor agonist, [Ala11, D-Leu15]orexin B. Orexin A attenuated the somato-Sympathetic Reflex but increased baroReflex sensitivity. Orexin A increased or reduced sympatho-excitation following hypoxia or hypercapnia respectively. CONCLUSIONS AND IMPLICATIONS Although central cardio-respiratory control mechanisms at rest do not rely on orexin, responses to adaptive stimuli are dramatically affected by the functional state of orexin receptors.
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intrathecal orexin a increases Sympathetic outflow and respiratory drive enhances baroReflex sensitivity and blocks the somato Sympathetic Reflex
British Journal of Pharmacology, 2011Co-Authors: Ahmed A Rahman, I Z Shahid, Paul M. PilowskyAbstract:BACKGROUND Intrathecal (i.t.) injection of orexin A (OX-A) increases blood pressure and heart rate (HR), but the effects of OX-A on Sympathetic and phrenic, nerve activity, and the baroReflex(es), somato-Sympathetic and hypoxic chemoReflex(es) are unknown. EXPERIMENTAL APPROACH Urethane-anaesthetized, vagotomized and artificially ventilated male Sprague-Dawley rats were examined in this study. The effects of i.t. OX-A (20 nmol 10 µL−1) on cardiorespiratory parameters, and responses to stimulation of the sciatic nerve (electrical), arterial baroreceptors (phenylephrine hydrochloride, 0.01 mg kg−1 i.v.) and peripheral (hypoxia) chemoreceptors were also investigated. KEY RESULTS i.t. OX-A caused a prolonged dose-dependent sympathoexcitation, pressor response and tachycardia. The peak effect was observed at 20 nmol with increases in mean arterial pressure, HR and splanchnic Sympathetic nerve activity (sSNA) of 32 mmHg, 52 beats per minute and 100% from baseline respectively. OX-A also dose-dependently increased respiratory drive, as indicated by a rise in phrenic nerve amplitude and a fall in phrenic nerve frequency, an increase in neural minute ventilation, a lengthening of the expiratory period, and a shortening of the inspiratory period. All effects of OX-A (20 nmol) were attenuated by the orexin receptor 1 antagonist SB 334867. OX-A significantly reduced both sympathoexcitatory peaks of somato-Sympathetic Reflex while increasing baroReflex sensitivity. OX-A increased the amplitude of the pressor response and markedly amplified the effect of hypoxia on sSNA. CONCLUSIONS Thus, activation of OX receptors in rat spinal cord alters cardiorespiratory function and differentially modulates Sympathetic Reflexes.
