Vestibulosympathetic Reflex Research Articles

Otolithic activation on visceral circulation in humans: effect of aging

Engagement of the otolith organs elicits differential activation of sympathetic nerve activity and vascular responses to muscle and skin in humans. Additionally, aging attenuates the otolith organ-mediated increases in muscle sympathetic nerve activity in older adults. In this study, we hypothesized that 1) the vestibulosympathetic reflex (VSR) would elicit visceral vascular vasoconstriction and 2) visceral vascular response to the VSR would be attenuated in older subjects compared with young. To test these hypotheses, heart rate, mean arterial blood pressure, and renal, celiac trunk, and superior mesenteric arterial blood velocity (Doppler ultrasound) were measured in 22 young (25+/-1 yr) and 18 older (65+/-2 yr) healthy subjects during head-down rotation (HDR), which selectively activates the otolith organs. Mean arterial pressure and heart rate did not change from baseline during HDR in young or older subjects. Renal blood velocity (Delta -2+/-1 cm/s) and vascular conductance (Delta -0.03+/-0.01 cm.s(-1).mmHg(-1)) significantly decreased from baseline during HDR (P<0.05) in young subjects. In contrast, renal blood velocity and conductance did not change in older subjects (Delta -0.2+/-1 cm/s and Delta0.02+/-0.08 mmHg.cm(-1).s(-1), respectively) during HDR. Superior mesenteric and celiac blood velocity and vascular conductance did not change in response to HDR in either the young or older subjects. These data suggest that renal vasoconstriction occurs during otolith organ activation in young but not older humans. Together with our previous studies, we conclude that the VSR elicits a diverse patterning of sympathetic outflow that results in heterogeneous vascular responses in humans and that these responses are significantly attenuated in older humans.

Greater sensitivity of the vestibulosympathetic reflex in the upright posture in humans

Otolith organs have been shown to activate the sympathetic nervous system in the prone position by head-down rotation (HDR) in humans. To date, otolithic stimulation by HDR has not been comprehensively studied in the upright posture. The purpose of the present study was to determine whether otolithic stimulation increases muscle sympathetic nerve activity (MSNA) in the upright posture. It was hypothesized that stimulation of the otolith organs would increase MSNA in the upright posture, despite increased baseline sympathetic activation due to unloading of the baroreceptors. MSNA, arterial blood pressure, heart rate, and degree of head rotation were measured during HDR in 18 volunteers (23 +/- 1 yr) in different postures. Study 1 (n = 11) examined HDR in the prone and sitting positions and study 2 (n = 7) examined HDR in the prone and 60 degrees head-up tilt positions. Baseline MSNA was 8 +/- 4, 15 +/- 4, and 33 +/- 2 bursts/min for prone, sitting, and head-up tilt, respectively. HDR significantly increased MSNA in the prone (Delta4 +/- 1 and Delta105 +/- 37% for burst frequency and total activity, respectively), sitting (Delta5 +/- 1 and Delta43 +/- 12%), and head-up tilt (Delta7 +/- 1 and Delta110 +/- 41%; P < 0.05). Sensitivity of the vestibulosympathetic reflex (%DeltaMSNA/DeltaHDR; degree of head rotation) was significantly greater in the sitting and head-up tilt than prone position (prone = 74 +/- 22; sitting = 109 +/- 30; head-up tilt = 276 +/- 103; P < 0.05). These data indicate that stimulation of the otolith organs can mediate increases in MSNA in the upright posture and suggest a greater sensitivity of the vestibulosympathetic reflex in the upright posture in humans.

Vestibulosympathetic reflex during the early follicular and midluteal phases of the menstrual cycle

Evidence suggests that both the arterial baroreflex and vestibulosympathetic reflex contribute to blood pressure regulation, and both autonomic reflexes integrate centrally in the medulla cardiovascular center. A previous report indicated increased sympathetic baroreflex sensitivity during the midluteal (ML) phase of the menstrual cycle compared with the early follicular (EF) phase. On the basis of this finding, we hypothesize an augmented vestibulosympathetic reflex during the ML phase of the menstrual cycle. Muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate responses to head-down rotation (HDR) were measured in 10 healthy females during the EF and ML phases of the menstrual cycle. Plasma estradiol (Delta72 +/- 13 pg/ml, P < 0.01) and progesterone (Delta8 +/- 2 ng/ml, P < 0.01) were significantly greater during the ML phase compared with the EF phase. The menstrual cycle did not alter resting MSNA, MAP, and heart rate (EF: 13 +/- 3 bursts/min, 80 +/- 2 mmHg, 65 +/- 2 beats/min vs. ML: 14 +/- 3 bursts/min, 81 +/- 3 mmHg, 64 +/- 3 beats/min). During the EF phase, HDR increased MSNA (Delta3 +/- 1 bursts/min, P < 0.02) but did not change MAP or heart rate (Delta0 +/- 1 mmHg and Delta1 +/- 1 beats/min). During the ML phase, HDR increased both MSNA and MAP (Delta4 +/- 1 bursts/min and Delta3 +/- 1 mmHg, P < 0.04) with no change in heart rate (Delta0 +/- 1 beats/min). MSNA and heart rate responses to HDR were not different between the EF and ML phases, but MAP responses to HDR were augmented during the ML phase (P < 0.03). Our results demonstrate that the menstrual cycle does not influence the vestibulosympathetic reflex but appears to alter MAP responses to HDR during the ML phase.

Glycerol‐induced fluid shift attenuates the vestibulosympathetic reflex in humans

Classically, the glycerol dehydration test (GDT) has been used to test for the presence of Ménière's disease and can cause acute alterations in vestibular reflexes in both normal and pathological states. The vestibulosympathetic reflex (VSR) elicits increases in muscle sympathetic nerve activity (MSNA) and peripheral vasoconstriction. We hypothesized that the GDT would attenuate the VSR through an acute fluid shift of the inner ear. Nine male subjects (27±1 years) performed head‐down rotation (HDR), which engages the VSR, before and after administration of either the GDT or saline. MSNA (microneurography), arterial blood pressure, and leg blood flow (venous occlusion plethysmography) were measured during HDR. Subjects performed 80‐degree head‐up tilt for up to 30 minutes after the post‐tests. Before drug administration, HDR significantly increased MSNA in burst frequency (Δ5±1 bursts/min, Δ8±1 bursts/min; p&lt;0.01) and total activity (Δ44±13% Δ77±17%; p&lt;0.01), and decreased calf vascular conductance (Δ15±6%, Δ20±3%; p&lt;0.01), in both the saline and glycerol trials, respectively. Post‐saline injection, HDR still significantly increased MSNA (Δ6±2 bursts/min, Δ83±20% total activity; p&lt;0.01) and decreased calf vascular conductance (Δ21±4%, p&lt;0.01), which was not significantly different from pretesting. In contrast, post‐GDT resulted in an attenuation of MSNA (Δ3±1 bursts/min, Δ22±3% total activity) and reduction in calf vascular conductance (Δ7±4%) during HDR. These results suggest that a fluid shift of the inner ear via glycerol dehydration attenuates the VSR. These data provide support that dynamic fluid shifts can have a significant effect on the VSR.Research supported by NIH DC006459, HL077670, &amp; M01RR10732 and NSBRI CA00404

Vestibulosympathetic reflex during the early follicular and mid‐luteal phases of the menstrual cycle

The influence of the menstrual cycle on the vestibulosympathetic reflex is unknown. We examined muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), and heart rate responses to head‐down rotation (HDR) in 10 healthy females during the early follicular (EF) and mid‐luteal (ML) phases of the menstrual cycle. The menstrual cycle had no effect on resting MSNA, MAP, and heart rate (EF: 13±3 bursts/min, 81±3 mmHg, 65±2 beats/min versus ML: 14+3 bursts/min, 83±3 mmHg, 64±3 beats/min). During the EF phase, HDR increased MSNA (Δ3±1 bursts/min; P&lt;0.05), but did not change MAP or heart rate (Δ0±1 mmHg and Δ1±1 beats/min). During the ML phase, HDR increased both MSNA and MAP (Δ4±1 bursts/min and Δ3±1 mmHg; P&lt;0.05) with no change in heart rate (Δ0±1 beats/min). MSNA and heart rate responses to HDR were not different between the EF and ML phases, but MAP responses to HDR were augmented during the ML phase (Interaction, P=0.029). Our results demonstrate that the menstrual cycle does not influence the vestibulosympathetic reflex, but appears to alter MAP responses to HDR during the ML phase. The augmented arterial blood pressure during the ML phase of the menstrual cycle may be due to increased sympathetic transduction to the vascular smooth muscle. Supported by REF‐060605.

Sympathetic responses to vestibular activation in humans

Activation of sympathetic neural traffic via the vestibular system is referred to as the vestibulosympathetic reflex. Investigations of the vestibulosympathetic reflex in humans have been limited to the past decade, and the importance of this reflex in arterial blood pressure regulation is still being determined. This review provides a summary of sympathetic neural responses to various techniques used to engage the vestibulosympathetic reflex. Studies suggest that activation of the semicircular canals using caloric stimulation and yaw rotation do not modulate muscle sympathetic nerve activity (MSNA) or skin sympathetic nerve activity (SSNA). In contrast, activation of the otolith organs appear to alter MSNA, but not SSNA. Specifically, head-down rotation and off-vertical axis rotation increase MSNA, while sinusoidal linear accelerations decrease MSNA. Galvanic stimulation, which results in a nonspecific activation of the vestibule, appears to increase MSNA if the mode of delivery is pulse trained. In conclusion, evidence strongly supports the existence of a vestibulosympathetic reflex in humans. Furthermore, attenuation of the vestibulosympathetic reflex is coupled with a drop in arterial blood pressure in the elderly, suggesting this reflex may be important in human blood pressure regulation.

Effect of baroreflex loading on the responsiveness of the vestibulosympathetic reflex in humans

Activation of the vestibular otolith organs with head-down rotation (HDR) increases muscle sympathetic nerve activity (MSNA) in humans. Previously, we demonstrated this vestibulosympathetic reflex (VSR) elicits increases in MSNA during baroreflex unloading (i.e., lower body negative pressure) in humans. Whether such an effect persists during baroreflex loading is unknown. We tested the hypothesis that the ability of the VSR to increase MSNA is preserved during baroreflex unloading and inhibited during baroreflex loading. Ten subjects (26 +/- 1 yr) performed three trials of HDR to activate the VSR. These trials were performed after a period of sustained saline (control), nitroprusside (baroreflex unloading: 0.8-1.0 microg.kg(-1).min(-1)), and phenylephrine (baroreflex loading: 0.6-0.8 microg.kg(-1).min(-1)) infusion. Nitroprusside infusion decreased (Delta7 +/- 1 mmHg, where Delta is change; P < 0.001) and phenylephrine infusion increased mean arterial pressure (Delta8 +/- 1 mmHg; P < 0.001) at rest. HDR performed during the control [Delta3 +/- 2 bursts/min, Delta314 +/- 154 arbitrary units (au) total activity, Delta41 +/- 18% total activity; P < 0.05] and nitroprusside trials [Delta5 +/- 2 bursts/min, Delta713 +/- 241 au total activity, Delta49 +/- 20% total activity; P < 0.05] increased MSNA similarly despite significantly elevated levels at rest (13 +/- 2 to 26 +/- 3 bursts/min) in the latter. In contrast, HDR performed during the phenylephrine trial failed to increase MSNA (Delta0 +/- 1 bursts/min, Delta-15 +/- 33 au total activity, Delta-8 +/- 21% total activity). These results confirm previous findings that the ability of the VSR to increase MSNA is preserved during baroreflex unloading. In contrast, the ability of the VSR to increase MSNA is abolished during baroreflex loading. These results provide further support for the concept that the VSR may act primarily to defend against hypotension in humans.

Effect of dimenhydrinate on autonomic activity in humans

The purpose of this study was to examine the effect of dimenhydrinate on resting muscle sympathetic nerve activity (MSNA), the vestibulosympathetic reflex, and the baroreflexes. Sixteen subjects participated in two double-blinded studies that measured mean arterial pressure (MAP), heart rate (HR), and MSNA responses before and after oral administration of dimenhydrinate (100 mg) or a placebo. In study one, 3 min of head-down rotation (HDR) was performed to engage the otolith organs. Dimenhydrinate (n = 10) did not alter resting MSNA, MAP, or HR. HDR increased MSNA before (Delta5 +/- 1 bursts/min; P < 0.01) and after (Delta4 +/- 1 bursts/min; P < 0.01) drug administration, but these responses were not different from the placebo (n = 6). In study two, 4 min of lower body negative pressure (LBNP) at -30 mmHg was performed. During the third min of LBNP, HDR was performed. MSNA increased during the first 2 min of LBNP before (Delta13 +/- 2 bursts/min; P < 0.01) and after (Delta14 +/- 2 bursts/min; P < 0.01) dimenhydrinate. HDR combined with LBNP increased MSNA further during the third min of LBNP (Delta18 +/- 2 bursts/min before and Delta17 +/- 2 bursts/min after dimenhydrinate; P < 0.01). These responses were not significantly different from the placebo. In contrast, HR responses to LBNP during the dimenhydrinate trial were increased when compared to all other trials (Delta5 +/- 1 beats/min; P < 0.01). These results indicate that dimenhydrinate augments heart rate responses to baroreceptor unloading, but does not alter resting MSNA, the sympathetic baroreflexes, or the vestibulosympathetic reflex.

Effect of dimenhydrinate on the vestibulosympathetic reflex and baroreflexes in humans

The purpose of this study was to examine the effect of dimenhydrinate on resting muscle sympathetic nerve activity (MSNA), the vestibulosympathetic reflex, and the baroreflexes. Sixteen subjects pa...

ENDURANCE TRAINING ATTENUATES THE VESTIBULOSYMPATHETIC REFLEX IN RUNNERS

A possible mechanism for exercise training-induced orthostatic intolerance is attenuation of the vestibulosympathetic reflex due to constant stimulation of the otolith organs during running. We tested the hypothesis that 8 weeks of endurance training will attenuate the vestibulosympathetic reflex in runners, but not stationary bikers. Arterial blood pressure, heart rate, calf blood flow, and muscle sympathetic nerve activity (MSNA) were recorded in healthy, sedentary, prone subjects (25±1 yr) at baseline and during head-down rotation (HDR) before and after 8 weeks of endurance training. Subjects were assigned to running (n=13), stationary biking (n=12), or time control (n=12) groups. HDR increased MSNA and decreased calf vascular conductance (CVC) significantly in all groups before training. In contrast, after training MSNA did not increase (p>0.05) during HDR in runners (Δ2±1 bursts/min from baseline), but did in bikers and controls (Δ5±1 and Δ4±2 bursts/min, respectively; p<0.05). Furthermore, CVC did not decrease from baseline with HDR in runners, but decreased in bikers and controls (p<0.001). These data suggest an attenuation of the vestibulosympathetic reflex in endurance-trained runners, but not stationary bikers. This is the first study to suggest that endurance running decreases the sensitivity of the otolith organs to changes in gravitational inputs. NIH DC006459, HL077670, and MO1RR10732

Endurance Training Attenuates Renal Artery Vasoconstriction During Vestibular Stimulation in Runners

Activation of the vestibulosympathetic reflex (VSR) elicits vasoconstriction in peripheral vascular beds to assist with blood pressure control. Endurance training has been associated with an increased incidence of orthostatic intolerance. We tested the hypothesis that endurance training will alter renal vascular conductance (RVC) through attenuation of the VSR in runners, but not stationary bikers through over stimulation of the otolith organs. 32 subjects (25±1 yr) were tested before and after 8 weeks of endurance training (11 runners, 12 bikers, 9 time controls). Arterial blood pressure, heart rate, and renal blood velocity (Doppler ultrasound) were recorded at baseline and during HDR in the prone position. VO2peak increased after training in both runners and bikers (Δ25±3% and Δ20±2%, respectively; p<0.001). Before training, all groups demonstrated a significant decrease in RVC (Δ−6±3%, Δ−12±4%, Δ −7±3%; runners, bikers, controls, respectively; p<0.05) during the first minute of HDR. However, after training HDR did not elicit a decrease in RVC in runners, unlike bikers and controls RVC (Δ−6±4%, Δ−7±3%, respectively; p<0.05). These data suggest that training modality alters VSR-mediated renal vasoconstriction by modifying the sensitivity of the otolith organs to gravitational inputs. NIH DC006459, HL077670, NSBRI CA00404 & MO1RR10732

Modeling baroreflex regulation of heart rate during orthostatic stress

During orthostatic stress, arterial and cardiopulmonary baroreflexes play a key role in maintaining arterial pressure by regulating heart rate. This study presents a mathematical model that can predict the dynamics of heart rate regulation in response to postural change from sitting to standing. The model uses blood pressure measured in the finger as an input to model heart rate dynamics in response to changes in baroreceptor nerve firing rate, sympathetic and parasympathetic responses, vestibulo-sympathetic reflex, and concentrations of norepinephrine and acetylcholine. We formulate an inverse least squares problem for parameter estimation and successfully demonstrate that our mathematical model can accurately predict heart rate dynamics observed in data obtained from healthy young, healthy elderly, and hypertensive elderly subjects. One of our key findings indicates that, to successfully validate our model against clinical data, it is necessary to include the vestibulo-sympathetic reflex. Furthermore, our model reveals that the transfer between the nerve firing and blood pressure is nonlinear and follows a hysteresis curve. In healthy young people, the hysteresis loop is wide, whereas, in healthy and hypertensive elderly people, the hysteresis loop shifts to higher blood pressure values, and its area is diminished. Finally, for hypertensive elderly people, the hysteresis loop is generally not closed, indicating that, during postural change from sitting to standing, baroreflex modulation does not return to steady state during the first minute of standing.

Cardiovascular modules in the cerebellum

Mapping with local lesions, electrical or chemical stimulation, or recording evoked field potentials or unit spikes revealed localized representations of cardiovascular functions in the cerebellum. In this review, which is based on literatures in the field (including our own publications), I propose that the cerebellum contains five distinct modules (cerebellar corticonuclear microcomplexes) dedicated to cardiovascular control. First, a discrete rostral portion of the fastigial nucleus and the overlying medial portion of the anterior vermis (lobules I, II and III) conjointly form a module that controls the baroreflex. Second, anterior vermis also forms a microcomplex with the parabrachial nucleus. Third, a discrete caudal portion of the fastigial nucleus and the overlying medial portion of the posterior vermis (lobules VII and VIII) form another module controlling the vestibulosympathetic reflex. Fourth, the medial portion of the uvula may form a module with the nucleus tractus solitarius and parabrachial nucleus. Fifth, the lateral edge of the nodulus and the uvula, together with the parabrachial nucleus and vestibular nuclei, forms a cardiovascular microcomplex that controls the magnitude and/or timing of sympathetic nerve responses and stability of the mean arterial blood pressure during changes of head position and body posture. The lateral nodulus-uvula appears to be an integrative cardiovascular control center involving both the baroreflex and the vestibulosympathetic reflex.

Electrical activation of the human vestibulo-sympathetic reflex

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.

Effect of examination stress on the alteration of blood pressure in young normotensives

It is known that stress alters mental status and biological processes. Acute mental stress due to stressful interviews increases blood pressure. To assess the effect of chronic stress due to preparation of examination on cardiovascular function. The blood pressure of young normotensive medical students (n=55) was measured using a mercury sphygmomanometer during a casual (less stressful) period and during the period of preparation for final examinations. Data were analysed by Student's t-test. In the period of preparation for final examinations a significant rise in diastolic and mean blood pressure took place in both sexes (P<0.05). The aforesaid result may be due to the vestibulo-sympathetic reflex elicited by head down and neck flexed posture (the conventional position of study) for a prolonged time.

Forearm neurovascular responses during mental stress and vestibular activation.

Autonomic responses may underlie associations among anxiety, vestibular dysfunction, and unexplained syncope. Mental stress (MS), an anxiety-inducing stimulus, causes forearm vasodilation, whereas the vestibulosympathetic reflex (VSR) causes forearm vasoconstriction. The purpose of this study was to examine the combined effects of mental and vestibular stimulation on neurovascular control in the forearm. Heart rate, arterial pressure (Finapres), and forearm blood flow (Doppler) were measured in 10 healthy volunteers in the prone position during 1) head-down rotation (HDR), 2) MS (mental arithmetic), and 3) HDR + MS. Forearm vascular resistance (FVR) increased during HDR (from 232 +/- 40 to 319 +/- 53 units) and decreased during MS (from 260 +/- 57 to 154 +/- 22 units). During HDR + MS, FVR did not change [change (Delta) = -31 +/- 50 units] and was not significantly different from the algebraic sum of each trial performed alone (Delta = -20 +/- 42 units). Arm muscle sympathetic nerve activity (MSNA; microneurography) was measured in seven additional subjects. MSNA increased during HDR (from 13 +/- 2 to 17 +/- 2 bursts/min) and HDR + MS (from 11 +/- 2 to 16 +/- 2 bursts/min). Increases in MSNA during HDR + MS (Delta = 5 +/- 2 bursts/min) were not different from the algebraic sum of each trial performed alone (Delta = 6 +/- 2 bursts/min). We conclude that an additive neurovascular interaction exists between MS and the VSR in the forearm. Activation of the VSR prevented forearm vasodilation during MS, suggesting that activation of the VSR may help protect against stress-induced syncope.

Vestibulosympathetic reflex mediates the pressor response to hypergravity in conscious rats: contribution of the diencephalon

To investigate the mechanism of arterial pressure (AP) regulation during hypergravity, the AP response to gravitational force was examined in conscious rats and the AP was found to increase, depending on the degree of gravity load induced by centrifugation. At 20 s after application of 2, 3, or 5 G, the AP increased by 9±2, 20±3, or 24±3 mm Hg, respectively. The AP increase during first 60 s was suppressed by vestibular lesion or pretreatment with hexamethonium, suggesting that the vestibular system and sympathetic nerve system be involved, respectively, in the afferent and efferent pathways. To further examine the central pathway of this response, Fos expression in the brain was examined after exposure to 5 G for 90 min. Intense Fos expression was seen in the medial vestibular nucleus, paraventricular hypothalamic nucleus, autonomic nuclei in the brain stem in intact rats, but not in rats with vestibular lesion. To examine the involvement of the diencephalic nuclei in this pressor response, AP was measured under hypergravity in rats with midcollicular transection. In these rats, the AP change was minimal at 2, 3, and 5 G, indicating that nuclei rostral to the transection level were involved in the pressor response. These results indicate that output from the vestibular system project to the diencephalon, and activation of diencephalic nuclei is indispensable to the pressor response via the sympathetic nerve system.

Vestibular activation does not influence skin sympathetic nerve responses during whole body heating.

The cutaneous vasculature and eccrine sweat glands are modified by both thermal and nonthermal factors. To determine the effect of thermal stress on the vestibulosympathetic reflex, skin sympathetic nerve activity (SSNA) and cutaneous end-organ responses were measured in 10 subjects during static head-down rotation (HDR) and dynamic yaw and pitch (30 cycles/min) to activate the otolith organs and semicircular canals. SSNA (microneurography of peroneal nerve), cutaneous vascular conductance (CVC; laser-Doppler flux/mean arterial pressure), sweat rate (capacitance hygrometry), and body temperature were collected during normothermia and after whole body heating. Body temperature was controlled by perfusing neutral (34-35 degrees C) or warm (44-46 degrees C) water through a tube-lined suit. During normothermia, HDR did not alter SSNA (-0.4 +/- 4.4% change), CVC (4.2 +/- 6.9% change), or sweat rate (-2.7 +/- 1.2% change) within the innervated area of skin. Dynamic yaw and pitch also did not elicit significant changes in SSNA, CVC, or sweat rate during normothermia. Whole body heating significantly increased internal temperature (0.8 +/- 0.1 degrees C), mean skin temperature (4.1 +/- 0.2 degrees C), CVC (322 +/- 109% control), and sweat rate (0.35 +/- 0.08 mg.cm(-2).min(-1)). After whole body heating, HDR did not significantly alter SSNA (3.2 +/- 7.6% change), CVC (-7.3 +/- 3.9% change), or sweat rate (-3.3 +/- 1.9% change). Dynamic yaw and pitch also did not produce significant changes in SSNA, CVC, or sweat rate after whole body heating. These data suggest that vestibular activation by head movements is not a nonthermal factor affecting SSNA and cutaneous end-organ responses in humans.

Cardiovascular Modules in the Cerebellum

Mapping with local lesions, electrical or chemical stimulation, or recording evoked field potentials or unit spikes revealed localized representations of cardiovascular functions in the cerebellum. In this review, which is based on literatures in the field (including our own publications), I propose that the cerebellum contains five distinct modules (cerebellar corticonuclear microcomplexes) dedicated to cardiovascular control. First, a discrete rostral portion of the fastigial nucleus and the overlying medial portion of the anterior vermis (lobules I, II and III) conjointly form a module that controls the baroreflex. Second, anterior vermis also forms a microcomplex with the parabrachial nucleus. Third, a discrete caudal portion of the fastigial nucleus and the overlying medial portion of the posterior vermis (lobules VII and VIII) form another module controlling the vestibulosympathetic reflex. Fourth, the medial portion of the uvula may form a module with the nucleus tractus solitarius and parabrachial nucleus. Fifth, the lateral edge of the nodulus and the uvula, together with the parabrachial nucleus and vestibular nuclei, forms a cardiovascular microcomplex that controls the magnitude and/or timing of sympathetic nerve responses and stability of the mean arterial blood pressure during changes of head position and body posture. The lateral nodulus-uvula appears to be an integrative cardiovascular control center involving both the baroreflex and the vestibulosympathetic reflex.

Roles of baroreflex and vestibulosympathetic reflex in controlling arterial blood pressure during gravitational stress in conscious rats.

Gravity acts on the circulatory system to decrease arterial blood pressure (AP) by causing blood redistribution and reduced venous return. To evaluate roles of the baroreflex and vestibulosympathetic reflex (VSR) in maintaining AP during gravitational stress, we measured AP, heart rate (HR), and renal sympathetic nerve activity (RSNA) in four groups of conscious rats, which were either intact or had vestibular lesions (VL), sinoaortic denervation (SAD), or VL plus SAD (VL + SAD). The rats were exposed to 3 G in dorsoventral axis by centrifugation for 3 min. In rats in which neither reflex was functional (VL + SAD group), RSNA did not change, but the AP showed a significant decrease (-8 +/- 1 mmHg vs. baseline). In rats with a functional baroreflex, but no VSR (VL group), the AP did not change and there was a slight increase in RSNA (25 +/- 10% vs. baseline). In rats with a functional VSR, but no baroreflex (SAD group), marked increases in both AP and RSNA were observed (AP 31 +/- 6 mmHg and RSNA 87 +/- 10% vs. baseline), showing that the VSR causes an increase in AP in response to gravitational stress; these marked increases were significantly attenuated by the baroreflex in the intact group (AP 9 +/- 2 mmHg and RSNA 38 +/- 7% vs. baseline). In conclusion, AP is controlled by the combination of the baroreflex and VSR. The VSR elicits a huge pressor response during gravitational stress, preventing hypotension due to blood redistribution. In intact rats, this AP increase is compensated by the baroreflex, resulting in only a slight increase in AP.