Simultaneous measurement of central amygdala neuronal activity and sympathetic nerve activity during daily activities in rats.

NEW FINDINGS: What is the central question of this study? The functional relationships between central amygdala neuronal activity (CeANA) and sympathetic nerve activity in daily activities remain unclear. We aimed to measure CeANA, renal and lumbar sympathetic nerve activity (RSNA and LSNA, respectively), heart rate (HR) and arterial pressure simultaneously in freely moving rats. What is the main finding and its importance? The CeANA was significantly related to RSNA and LSNA and HR in a behavioural state-dependent and regionally different manner; meanwhile, CeANA was tightly associated with RSNA and HR across all behavioural states. Thus, it is likely that the amygdala is a component of neural networks generating regional differences in RSNA and LSNA. ABSTRACT: The central amygdala (CeA) is involved in generating diverse changes in sympathetic nerve activity (SNA) in response to changes in daily behavioural states. However, the functional relationships between CeA neuronal activity (CeANA) and SNA in daily activities are still unclear. In the present study, we developed a method for simultaneous and continuous measurement of CeANA and SNA in freely moving rats. Wistar rats were chronically instrumented with multiple electrodes (100-µm-thick stainless-steel wire) for the measurement of CeANA, renal SNA (RSNA) and lumbar SNA (LSNA), and electroencephalogram, EMG and ECG electrodes, in addition to catheters for measurement of arterial pressure (AP). During the transition from non-rapid eye movement sleep to quiet wakefulness, moving and grooming states, a significant linear relationship was observed between CeANA and RSNA (P < 0.0001), between CeANA and LSNA (P = 0.0309), between CeANA and heart rate (HR) (P = 0.0123) and between CeANA and EMG (P = 0.0089), but no significant correlation was observed between CeANA and AP (P = 0.5139). During rapid eye movement sleep, the relationships between CeANA and RSNA, LSNA, HR, AP and EMG deviated from the previously observed linear relationships, but the time course of RSNA and HR changes was the mirror image of that of CeANA, whereas the time course of changes in LSNA and AP was not related to that of CeANA. In conclusion, CeANA was related to RSNA, LSNA and HR in a behavioural state-dependent and regionally different manner, and CeANA was tightly associated with RSNA and HR across all behavioural states.

Regional Differences in Sympathetic Nerve Activity Are Generated by Multiple Arterial Baroreflex Loops Arranged in Parallel.

In this review, by evaluating the responses during freezing, rapid eye movement (REM) sleep, and treadmill exercise, we discuss how multiple baroreflex loops arranged in parallel act on different organs to modulate sympathetic nerve activity (SNA) in a region-specific and coordinated manner throughout the body. During freezing behaviors, arterial pressure (AP) remains unchanged, heart rate (HR) persistently decreases, renal SNA (RSNA) increases, and lumbar SNA (LSNA) remains unchanged. The baroreflex curve for RSNA shifts upward; that for LSNA remains unchanged; and that for HR shifts to the left. These region-specific changes in baroreflex curves are responsible for the region-specific changes in RSNA, LSNA, and HR during freezing. The decreased HR could allow the heart to conserve energy, which is offset by the increased RSNA caused by decreased vascular conductance, resulting in an unchanged AP. In contrast, the unchanged LSNA leaves the muscles in readiness for fight or flight. During REM sleep, AP increases, RSNA and HR decrease, while LSNA is elevated. The baroreflex curve for RSNA during REM sleep is vertically compressed in comparison with that during non-REM sleep. Cerebral blood flow is elevated while cardiac output is decreased during REM sleep. To address this situation, the brain activates the LSNA selectively, causing muscle vasoconstriction, which overcomes vasodilation of the kidneys as a result of the decreased RSNA and cardiac output. Accordingly, AP can be maintained during REM sleep. During treadmill exercise, AP, HR, and RSNA increase simultaneously. The baroreflex curve for RSNA shifts right-upward with the increased feedback gain, allowing maintenance of a stable AP with significant fluctuations in the vascular conductance of working muscles. Thus, the central nervous system may employ behavior-specific scenarios for modulating baroreflex loops for differential control of SNA, changing the SNA in a region-specific and coordinated manner, and then optimizing circulatory regulation corresponding to different behaviors.

Differential shifts in baroreflex control of renal and lumbar sympathetic nerve activity induced by freezing behaviour in rats.

NEW FINDINGS: What is the central question of this study? Is the arterial baroreflex involved in causing patterned, region-specific changes in sympathetic nerve activity during freezing behaviour in conscious rats? What is the main finding and its importance? Freezing behaviour is accompanied by differential shifts in the baroreflex control of renal and lumbar sympathetic nerve activity and heart rate. It is noteworthy that baroreflex pathways may be discretely separated, allowing differential modification of baroreflex curves that may generate differential changes in sympathetic nerve activity during freezing behaviour. ABSTRACT: The present study was designed to test whether the baroreflex stimulus-response curves for renal sympathetic nerve activity (RSNA), lumbar sympathetic nerve activity (LSNA) and heart rate (HR) were shifted in a regionally specific manner during freezing behaviour in conscious rats. Male Wistar rats were chronically instrumented with electrodes and arterial and venous catheters for measurement of RSNA, LSNA and electrocardiogram. After a 60-min control period, freezing behaviour in conscious rats was induced by exposure to loud white noise (90 dB) for 10 min. The baroreflex curves for RSNA, LSNA and HR were generated by changing systemic arterial pressure using rapid intravenous infusions of vasoactive drugs and then fitted to an inverse sigmoid function curve. During the freezing behaviour, the baroreflex curve for RSNA was expanded upward with a significant (P < 0.001) increase (by 153% compared with the control level) in the upper plateau (maximum capacity of RSNA drive), whereas the baroreflex curve for LSNA remained unchanged. Conversely, the baroreflex curve for HR was shifted leftward with a significant (P = 0.004) decrease (by 11 mmHg relative to the control level) in the midpoint pressure. Our results indicate that baroreflex curve shifts for RSNA, LSNA and HR occur in a regionally specific manner during freezing behaviour. This indicates that baroreflex pathways may be discretely separated, allowing differential modification of baroreflex curves that may generate differential changes in sympathetic nerve activity during freezing behaviour.

Renal and Lumbar Sympathetic Nerve Activity During Development of Hypertension in Dahl Salt-Sensitive Rats.

To study the contribution of sympathetic nerve activity (SNA) to the development of hypertension, experiments were designed to continuously and simultaneously measure renal (RSNA) and lumbar SNA (LSNA) during the development of hypertension induced by 8% salt loading in Dahl salt-sensitive (DS) rats. Male DS and salt-resistant rats were instrumented with bipolar electrodes to record RSNA and LSNA and a telemeter to record arterial pressure (AP). AP increased during the first 3 days after the onset of salt loading by ≈10 mm Hg in both DS and Dahl salt-resistant rats. AP continued to increase progressively from day 4 to day 14 of salt loading by 33±1 mm Hg in DS rats, while it remained the same in Dahl salt-resistant rats. RSNA and LSNA increased in the initial few days by 6% to 8%, and decreased gradually thereafter, suggesting that increases in neither RSNA nor LSNA are directly linked with the progressive increase in AP induced by salt loading in DS rats. After the cessation of salt loading, AP pressure returned to the presalt loading level in both DS and Dahl salt-resistant rats. RSNA increased significantly by 32±3% after the cessation of salt loading, while LSNA remained the same in DS rats, suggesting that salt-sensitive mechanisms respond to a loss of sodium, not a gain, and selectively activate RSNA in DS rats. In summary, RSNA and LSNA are not likely to be a primary trigger to initiate the progressive increase in AP induced by 8% salt loading in DS rats.

Exercise-Induced Modulation of Baroreflex Control of Sympathetic Nerve Activity.

Exercise modulates arterial pressure (AP) regulation over various time spans. AP increases at the onset of exercise and this increase is then sustained during exercise. Once exercise is stopped, AP is suppressed for up to an hour afterwards. Prolonged endurance training is associated with dysfunction of the sympathetic regulation of AP in response to posture changes (orthostatic intolerance). Baroreflex control of sympathetic nerve activity (SNA) has been extensively studied to understand the mechanisms underlying exercise-induced changes in AP. We have previously presented entire baroreflex AP-SNA curves during and after exercise, and during central volume expansion, obtained using direct measurements of renal sympathetic nerve activity (RSNA) in conscious animals. In this review, we describe the modulatory effects of exercise on baroreflex control of AP based on these entire AP-RSNA baroreflex curves. We suggest that both acute and chronic exercise can have modulatory effects on the entire baroreflex curve for SNA, and that these effects differ among time periods.

Reprint of "Sympathetic nerve activity during sleep, exercise, and mental stress".

This brief review describes recent findings on the differential regulation of sympathetic nerve activity and its role in regulating systemic arterial pressure during rapid eye-movement sleep, non-rapid-eye movement sleep, exercise and freezing behavior (mental stress). We describe the mechanisms underlying the differential regulation of sympathetic outflows and how they act in concert to orchestrate adjustments of cardiovascular function for the whole body, which are optimized to match changes in organ activity in daily activity.

Sympathetic nerve activity during sleep, exercise, and mental stress.

This brief review describes recent findings on the differential regulation of sympathetic nerve activity and its role in regulating systemic arterial pressure during rapid eye-movement sleep, non-rapid-eye movement sleep, exercise and freezing behavior (mental stress). We describe the mechanisms underlying the differential regulation of sympathetic outflows and how they act in concert to orchestrate adjustments of cardiovascular function for the whole body, which are optimized to match changes in organ activity in daily activity.

Functional role of diverse changes in sympathetic nerve activity in regulating arterial pressure during REM sleep.

STUDY OBJECTIVES: This study aimed to investigate whether REM sleep evoked diverse changes in sympathetic outflows and, if so, to elucidate why REM sleep evokes diverse changes in sympathetic outflows. MEASUREMENTS: Male Wistar rats were chronically implanted with electrodes to measure renal (RSNA) and lumbar sympathetic nerve activity (LSNA), electroencephalogram, electromyogram, and electrocardiogram, and catheters to measure systemic arterial and central venous pressure; these parameters were measured simultaneously and continuously during the sleep-awake cycle in the same rat. RESULTS: REM sleep resulted in a step reduction in RNSA by 36.1% ± 2.7% (P < 0.05), while LSNA increased in a step manner by 15.3% ± 2% (P < 0.05) relative to the NREM level. Systemic arterial pressure increased gradually (P < 0.05), while heart rate decreased in a step manner (P < 0.05) during REM sleep. In contrast to REM sleep, RSNA, LSNA, systemic arterial pressure, and heart rate increased in a unidirectional manner associated with increases in physical activity levels in the order from NREM sleep, quiet awake, moving, and grooming state. Thus, the relationship between RSNA vs. LSNA and systemic arterial pressure vs. heart rate observed during REM sleep was dissociated compared with that obtained during the other behavioral states. CONCLUSIONS: It is suggested that the diverse changes in sympathetic outflows during REM sleep may be needed to increase systemic arterial pressure by balancing vascular resistance between muscles and vegetative organs without depending on the heart.

Differential control of renal and lumbar sympathetic nerve activity during freezing behavior in conscious rats.

The present study was designed to document changes in sympathetic nerve activity and cardiovascular function when conscious rats were challenged with a noise stressor to induce freezing behavior. The potential contribution of the arterial baroreceptors in regulating sympathetic nerve activity and cardiovascular adjustments during the freezing behavior was then examined. Wistar male rats were assigned to sham-operated (SO) and sinoaortic-denervated (SAD) groups and instrumented chronically with electrodes for measurements of renal (RSNA) and lumbar (LSNA) sympathetic nerve activity, electroencephalogram, electromyogram, and electrocardiogram and catheters for measurements of systemic arterial and central venous pressure. Both SO and SAD rats were exposed to 90 dB of white noise for 10 min, causing freezing behavior in both groups. In SO rats, freezing behavior was associated with an immediate and significant (P < 0.05) increase in RSNA, no changes in LSNA or mean arterial pressure, and a significant (P < 0.05) decrease in heart rate. SAD attenuated the magnitude of the immediate increase in RSNA and had no influence on the response in LSNA during freezing behavior compared with SO rats. Moreover, in SAD rats, mean arterial pressure increased significantly (P < 0.05) while heart rate did not change during the freezing behavior. These data indicate that freezing behavior evokes regionally different changes in sympathetic outflows, which may be involved in generating the patterned responses of cardiovascular function to stressful or threatening sensory stimulation. Moreover, it is suggested that the arterial baroreceptors are involved in generating the differential changes in RSNA and LSNA and thus the patterned changes in cardiovascular functions observed during freezing behavior in conscious rats.

Chronic angiotensin II infusion causes differential responses in regional sympathetic nerve activity in rats.

Angiotensin II (AngII)-induced hypertension in experimental animals has been proposed to be attributed in part to activation of the sympathetic nervous system. This sympathetic activation appears to be accentuated in animals consuming a high-salt diet (AngII-salt hypertension). However, accurate quantification of sympathetic activity is difficult, and controversy remains. It is particularly important to ask which are the critical vascular beds targeted by increased sympathetic nerve activity (SNA) in AngII-salt hypertension. To address this issue, mean arterial pressure and renal SNA or lumbar SNA were continuously recorded during a 5-day control period, 11 days of AngII (150 ng/kg per minute, SC), and a 5-day recovery period in conscious rats on a high-salt (2% NaCl) diet. Although mean arterial pressure reached a new steady-state level of 30 to 35 mm Hg above control levels by the end of the AngII period, renal SNA decreased by 40% during the first 7 days of AngII and then returned toward control levels by day 10 of AngII. In contrast, lumbar SNA remained at control levels throughout the AngII period. In another experiment we measured hindlimb norepinephrine spillover in conscious rats on normal (0.4%) or high- (2.0%) salt diets before and during 14 days of AngII administration. AngII had no significant affect on hindlimb norepinephrine spillover in either group. We conclude that chronic AngII modulates renal and lumbar SNAs differentially in rats consuming a high-salt diet and that AngII-salt hypertension in the rat is not caused by increased SNA to the renal or hindlimb vascular beds.

Role of differential changes in sympathetic nerve activity in the preparatory adjustments of cardiovascular functions during freezing behaviour in rats.

Freezing behaviour is associated with a distinct pattern of changes in cardiovascular function, which has been considered as a preparatory reflex for 'fight or flight' behaviour. However, the detailed mechanisms underlying preparatory cardiovascular adjustments and their physiological implications have received less attention. We studied responses in renal and lumbar sympathetic nerve activity and cardiovascular function during freezing behaviour in conscious rats, which was induced by exposure to loud white noise. Freezing behaviour was associated with regionally specific alterations in sympathetic nerve activity, in that renal sympathetic nerve activity increased while lumbar sympathetic nerve activity did not change. Moreover, freezing behaviour was associated with differential shifts in baroreflex control of sympathetic outflows, which could help to explain the selective responses in renal and lumbar sympathetic nerve activity during freezing behaviour. These differential changes in sympathetic outflows would result in a visceral vasoconstriction without having any impact on the skeletal muscle vasculature. These cardiovascular adjustments during freezing behaviour may help to explain the immediate and massive increase in muscular blood flow that occurs at the onset of fight or flight behaviour. It is hypothesized that central command originating from the defence area could somehow modulate separate baroreflex pathways, causing differential changes in sympathetic nerve activity to generate the preparatory cardiovascular adjustments during the freezing behaviour.

Role of cardiopulmonary and carotid sinus baroreceptors in regulating renal sympathetic nerve activity during water immersion in conscious dogs.

The aim of the present study was to investigate how loading of cardiopulmonary baroreceptors induced by water immersion (WI) modifies baroreflex control of renal sympathetic nerve activity (RSNA) in conscious dogs. Nine dogs were chronically instrumented for measuring carotid sinus nerve activity (CSNA), RSNA, carotid arterial (Pca), and central venous (Pcv) pressures. The stimulus-response relationships of Pca-CSNA and Pca-RSNA were determined simultaneously in the same dog by changing Pca using rapid intravenous infusions vasoactive drugs during pre-WI and WI. WI increased central venous pressure significantly (P < 0.05) by 10.4 mmHg. WI shifted the Pca-RSNA curve acutely leftward compared with the pre-WI period, which was associated with significant (P < 0.05) decreases in the saturation pressure by 39.0 mmHg and operating range by 43.1 mmHg. WI relocated the operating pressure to near the saturation pressure, where the gain was low. The Pca-CSNA curve obtained during WI was identical to that obtained during pre-WI period. These results suggest that the shift in baroreflex control of RSNA could be attributed to the inhibitory influence of the cardiopulmonary mechanoreceptor loading and not by the resetting of carotid baroreceptors per se.

The contribution of brain angiotensin II to the baroreflex regulation of renal sympathetic nerve activity in conscious normotensive and hypertensive rats.

Angiotensin II receptor density in the brain is elevated when dietary salt intake is raised or in the state of hypertension. The aim of this study was to evaluate whether the angiotensin II modulation of the baroreceptor control of renal sympathetic nerve activity was altered under these conditions. Wistar rats, fed either a regular (0.25% w/w sodium) or high-salt diet (3.1% w/w sodium), or stroke-prone spontaneously hypertensive rats (SHRSPs) were implanted with cannulae in the carotid artery, jugular vein and the cerebroventricle and with recording electrodes on the renal sympathetic nerves. Three days later, baroreceptor gain curves were generated for renal sympathetic nerve activity and heart rate before and following intracerebroventricular (i.c.v.) administration of losartan (15 mug) to block angiotensin AT1 receptors. The rats fed a regular diet had a mean blood pressure of 116 +/- 3 mmHg and heart rate of 467 +/- 25 beats min(-1), which remained unchanged after the i.c.v. administration of losartan. The sensitivity or curvature coefficient of the baroreceptor curve for renal sympathetic nerve activity was increased by 36% (P < 0.05) following losartan. In the rats fed a high-salt diet, all cardiovascular variables and the losartan-induced increase in the baroreceptor curvature coefficient for renal sympathetic nerve activity (29%) were similar to values in rats on the regular sodium diet. The heart rate baroreceptor curvature coefficient was not altered in either the rats fed a regular or a high-salt diet. The slope of the renal sympathetic nerve activity baroreflex gain curve in the SHRSPs was less and the increase following administration of losartan (54%) was greater than in the Wistar rats. These data indicate that in the conscious state, the tonic inhibitory action of brain angiotensin II on the baroreflex regulation of renal sympathetic nerve activity was unaffected by raised dietary sodium, but its role was enhanced in the SHRSPs.

Differential effects of behaviour on sympathetic outflow during sleep and exercise.

The responses of renal and lumbar sympathetic outflow to changes in behavioural states were reviewed in this paper. During rapid eye movement (REM) sleep, renal sympathetic nerve activity was decreased while lumbar sympathetic nerve activity increased. These diverse changes in sympathetic nerve activity observed during REM sleep help explain the responses in regional blood flow to REM sleep; that is renal blood flow increased while muscle blood flow decreased. By contrast, exercise increased both renal and muscle sympathetic nerve activity. The degree of physical activity was correlated with the magnitude of the increases in renal and muscle sympathetic nerve activity. There was a significant (P<0.05) linear relationship between renal sympathetic nerve activity and systemic arterial pressure over the transition between non-rapid eye movement (NREM) sleep, quiet awake, moving and grooming states in the rats. This suggests that sympathetic outflows seem to be modulated quantitatively to meet cardiovascular demand caused by changes in the level of physical activity. It is therefore concluded that sympathetic outflow seems to be regulated in a state-specific manner during sleep and exercise.

Acute shifts in baroreflex control of renal sympathetic nerve activity induced by REM sleep and grooming in rats.

The present study aimed to determine the impact of REM sleep and grooming on the baroreflex stimulus-response curve for renal sympathetic nerve activity (RSNA). At least 3 days before study, Wistar female rats (n= 12) were chronically implanted with catheters to measure systemic arterial pressure (P(a)) and to intravenously infuse vasoactive drugs. In addition, electrodes were placed for measurements of RSNA, electroencephalogram, trapezius electromyogram and electrocardiogram. The baroreflex curve for RSNA was determined by changing P(a) using rapid intravenous infusions of phenylephrine and nitroprusside and then fitted to an inverse sigmoid function curve. REM sleep induced a vertical suppression of the P(a)-RSNA baroreflex curve, which was characterized by significant decreases in the maximum response (by 72.0%, P < 0.05) and the maximum gain (by 4.02% mmHg(-1), P < 0.05) compared with NREM sleep level. Grooming shifted the P(a)-RSNA baroreflex curve upward and to the right, which was associated with increases in the maximum response (by 45.2%, P < 0.05), the minimum response (by 20.7%, P < 0.05) and the pressure at the centering point (by 11.1 mmHg, P < 0.05). These data suggest that the P(a)-RSNA baroreflex curve was shifted acutely and differently in a state-dependent manner during natural sleep and wake cycle in rats.

Regulation of gastric motility at simulated high altitude in conscious rats.

The aim of the present study was to examine the effects of acute exposure to hypobaric hypoxia on gastric and colonic motilities. Wistar rats, which were instrumented chronically with strain gauge force transducer to measure gastric and colonic motilities, were exposed acutely to hypobaric hypoxia [0.5 atmosphere absolute (ATA, 380 Torr)] over 1 h. In a separate group, the gastric branches of the vagal nerves were cut and underwent the same experimental protocol. Each contraction wave of the stomach and colon was analyzed into frequency and area under the curves, which were then averaged every 10 min. Acute exposure to 0.5 ATA resulted in significant (P < 0.05) decreases in frequency and area of gastric contraction wave by 0.5 +/- 0.1 cycles/min and 64.6 +/- 4.0%, respectively. Gastric vagotomy abolished completely the suppression in the area observed in the intact rats during the 0.5-ATA exposures. Colonic motility increased significantly only at the start and end of exposure to 0.5 ATA and sham exposure [1 ATA (760 Torr), time control] in both intact and vagotomized rats. These data suggest that the acute suppression of the area of the gastric contraction wave that occurred during 0.5-ATA exposure is likely to be mediated by the vagal nerve.

Lumbar sympathetic nerve activity and hindquarter blood flow during REM sleep in rats.

The present study aimed to investigate the response of lumbar sympathetic nerve activity (LSNA) to the onset of rapid eye movement (REM) sleep and its contribution to the regulation of muscle blood flow during REM sleep in rats. Electrodes for the measurements of LSNA, electroencephalogram, electromyogram and electrocardiogram and a Doppler flow cuff for the measurements of blood flow in the common iliac and mesenteric arteries, also catheters for the measurements of systemic arterial and central venous pressures were implanted chronically. REM sleep resulted in a step increase in LSNA, by 22 +/- 9% (mean +/-S.E.M., P < 0.05), a reduction of iliac vascular conductance, by -16 +/- 3% (P < 0.05) and a gradual increase in systemic arterial pressure, reaching a maximum value of 8.1 +/- 2.0 mmHg (P < 0.05) at 89 s after onset of REM sleep, while mesenteric vascular conductance increased simultaneously by 5 +/- 2% (P < 0.05). There was a significant (Pearson's correlation coefficient = 0.94, P < 0.05) inverse linear relationship between LSNA and the iliac blood flow. Unilateral lumbar sympathectomy blunted the reduction of iliac blood flow induced by the onset of REM sleep. The present observations suggest that the onset of REM sleep appears to be associated with a vasodilation in viscera and a vasoconstriction in skeletal muscle, such that systemic arterial pressure increases during REM sleep in rats.

Relationship between renal sympathetic nerve activity and renal blood flow during natural behavior in rats.

The purpose of the present study was to determine the relationship between renal sympathetic nerve activity (RSNA) and renal blood flow (RBF) during normal daily activity in conscious, chronically instrumented Wistar rats (n = 8). The animal's behavior was classified as rapid eye movement (REM) sleep, non-REM (NREM) sleep, quiet awake, moving, and grooming states. On average RSNA was lowest during REM sleep, which was decreased by 39.0 +/- 3.2% (P < 0.05) relative to NREM sleep, and rose linearly with an increase in activity level in the order of quiet awake (by 10.9 +/- 1.8%, P < 0.05), moving (by 29.4 +/- 2.9%, P < 0.05), and grooming (by 65.3 +/- 3.9%, P < 0.05) relative to NREM sleep. By contrast, RBF was highest during REM sleep, which was increased by 4.8 +/- 0.7% (P < 0.05) relative to NREM sleep and decreased significantly (P < 0.05) by 5.5 +/- 0.6 and 6.6 +/- 0.5% during moving and grooming states, respectively, relative to NREM sleep. There was a significant (P < 0.05) inverse linear relationship between the percent changes in RSNA and RBF and between those in RSNA and renal vascular conductance. Furthermore, renal denervation (n = 8) abolished the changes in RBF induced by different natural behavioral activities. These results suggest that the changes in RSNA induced by natural behavioral activities had a significant influence on RBF.

Acute shifts of baroreflex control of renal sympathetic nerve activity induced by treadmill exercise in rats.

The present study aimed to investigate whether there was a resetting of the baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) during exercise. Wistar female rats (n = 11) were chronically implanted with catheters for the measurement of systemic arterial (Pa) and central venous pressures and with electrodes for measurement of RSNA and electrocardiogram (ECG) at least 3 days before study. The baroreflex curve for RSNA was determined by changing Pa using rapid intravenous infusions of phenylephrine and nitroprusside. The baroreflex response curves for RSNA and HR were characterized by an inverse sigmoid function curve from which the response range, gain, centering point and minimum response were estimated. Exercise shifted the Pa-RSNA baroreflex curve upward and to the right and was associated with increases in response range of 122 +/- 44 % (P < 0.05), maximum response of 173 +/- 40 % (P < 0.05), maximum gain of 149 +/- 66 % (P < 0.05) and midpoint pressure of 15 +/- 5 mmHg (P < 0.05) compared with the pre-exercise level. After cessation of exercise, the Pa-RSNA baroreflex curve was suppressed vertically with a significant decrease in maximum response of 57 +/- 14 % (P < 0.05) compared with the pre-exercise level. These data suggest that the right-upward shift of baroreflex control of sympathetic nerve activity may play a critical role in raising and stabilizing Pa during exercise. The suppression of the baroreflex control of sympathetic nerve activity may partly explain the post-exercise inhibition of sympathetic nerve activity and contribute to the post-exercise hypotension.

Relationship between renal sympathetic nerve activity and arterial pressure during REM sleep in rats.

The relationship between renal sympathetic nerve activity (RSNA) and systemic arterial pressure obtained during rapid eye movement (REM) sleep was compared with that obtained in other sleep and awake states. Electrodes for the measurements of RSNA, electrocardiogram, electromyogram, and electroencephalogram and a catheter for the measurement of systemic arterial pressure were implanted while the animals were under aseptic conditions at least 5 days before the experiment. During the transition from non-REM (NREM) to REM sleep, RSNA and heart rate (HR) decreased immediately by 46 +/- 2% (P < 0.05) and 22 +/- 3 beats/min (P < 0.05), respectively, over 3 s after the onset of REM sleep. Meanwhile, systemic arterial pressure increased gradually after the onset of REM sleep, which was apparently independent of the changes in RSNA. During REM sleep, the relationships between RSNA/HR and systemic arterial pressure were dissociated compared with that obtained during the other behavioral states. These data indicate that the interdependency between systemic arterial pressure and RSNA during REM sleep is likely to be modified compared with other behavioral states.