Sites at which vasopressin facilitates baroreflex inhibition of lumbar sympathetic nerve activity

1986 ◽  
Vol 251 (3) ◽  
pp. H644-H655 ◽  
Author(s):  
G. B. Guo ◽  
P. G. Schmid ◽  
F. M. Abboud
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Central Action ◽  
Nerve Activity ◽  
Arterial Baroreceptors ◽  
Aortic Depressor Nerve ◽  
Carotid Baroreflex ◽  
Vagal Nerves

We recently reported that intravenous vasopressin in anesthetized rabbits facilitates baroreflex inhibition of lumbar sympathetic nerve activity. The purpose of this study was to determine the possible sites of this facilitation. We found that intravenous infusion of vasopressin (16-32 mU X kg-1 X min-1) caused greater inhibition of lumbar sympathetic nerve activity than did phenylephrine for a given increase in aortic baroreceptor activity, suggesting a "central" action of vasopressin. A central action was supported also by the observation that the carotid baroreflex inhibition of lumbar sympathetic nerve activity was augmented by intravenous infusion of vasopressin when the carotid sinuses were isolated, filled with saline, and distended (aortic depressor and vagal nerves were cut). On the other hand, vasopressin also facilitated baroreflex inhibition of lumbar sympathetic nerve activity through an influence on arterial baroreceptors, because intravenous vasopressin caused greater afferent activity of the aortic depressor nerve per unit rise in arterial pressure than did phenylephrine. In a separate group of rabbits, intravenous infusion of vasopressin also elevated the level of afferent aortic depressor activity during increases in arterial pressure induced by intra-aortic balloon inflation. Furthermore, when vasopressin was confined to the isolated carotid sinuses, the reflex inhibition of lumbar sympathetic nerve activity during distension of carotid sinuses was augmented. We conclude that circulating vasopressin facilitates baroreflex inhibition of sympathetic nerve activity through a central nervous system action as well as through an effect on arterial baroreceptors.

Effect of vasopressin on baroreflex control of lumbar sympathetic nerve activity and hindquarter resistance

1996 ◽  
Vol 270 (6) ◽  
pp. H1963-H1971 ◽  
Author(s):  
D. A. Scheuer ◽  
V. S. Bishop
Keyword(s):  
Arterial Pressure ◽  
Vascular Resistance ◽  
Sympathetic Nerve ◽  
Intravenous Infusion ◽  
Sympathetic Nerve Activity ◽  
Area Postrema ◽  
Resistance Index ◽  
Inhibitory Influence ◽  
Nerve Activity ◽  
Baroreflex Control

Arginine vasopressin (AVP) has been shown to increase the inhibitory influence of the baroreflex on sympathetic nerve activity by a mechanism involving receptors located in the area postrema. The purpose of these experiments was to study the functional effect of this action of AVP by testing the hypothesis that AVP can buffer its own vasoconstrictor effect by facilitating baroreflex-mediated withdrawal of sympathetic nerve activity. Specifically, we determined 1) if AVP can attenuate increases in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine, and 2) whether the effects of AVP on vascular resistance are associated with appropriate corresponding changes in lumbar sympathetic nerve activity (LSNA). In pentobarbital-anesthetized New Zealand White rabbits the baroreflex was stimulated by phenylephrine-induced elevations in arterial pressure. Baroreflex-mediated changes in heart rate (HR), calculated hindquarter vascular resistance index (R), and LSNA were determined during the simultaneous intravertebral infusion of AVP (0, 0.5, or 1.0 ng.kg-1, min-1). Intravertebral infusion of AVP alone had no effect on resting mean arterial pressure (MAP) but reduced baseline values for LSNA and HR. Intravenous infusion of phenylephrine alone produced dose-dependent increases in MAP and R and decreases in LSNA and HR. The simultaneous infusion of AVP (0.5 or 1.0 ng.kg-1 min-1) and phenylephrine (1.25, 2.5, 5.0, 7.5, and 10.0 micrograms.kg-1.min-1) had no effect on the increase in MAP but attenuated the increases in R and facilitated the reductions in LSNA at all doses of phenylephrine. The higher dose of AVP also enhanced the phenylephrine-induced reductions in HR. In contrast, the intravenous infusion of AVP (1.0 ng.kg-1.min-1) did not alter baroreflex-mediated changes in R, LSNA, or HR. Therefore, we conclude that the action of AVP to increase baroreflex-mediated sympathoinhibition results in an attenuated rise in hindquarter vascular resistance during the infusion of another vasoconstrictor, phenylephrine.

Lateral parabrachial nucleus modulates baroreflex regulation of sympathetic nerve activity

1998 ◽  
Vol 274 (5) ◽  
pp. R1274-R1282 ◽  
Author(s):  
Linda F. Hayward ◽  
Robert B. Felder
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Chemical Activation ◽  
Parabrachial Nucleus ◽  
Nerve Activity ◽  
Baroreflex Control ◽  
Aortic Depressor Nerve ◽  
Descending Modulation ◽  
Lateral Parabrachial Nucleus

Previous studies have demonstrated that the lateral parabrachial nucleus (LPBN) is an important site for descending modulation of baroreflex control of heart rate. In the present study it was hypothesized that the LPBN neurons may also modulate baroreflex control of arterial pressure and sympathetic nerve activity. In urethan-anesthetized rats, electrical or chemical activation of the LPBN produced a significant reduction in the magnitude of the baroreflex inhibition of mean arterial pressure (MAP) and renal sympathetic nerve activity (RSNA) elicited by aortic depressor nerve stimulation. Chemical inactivation of the LPBN resulted in a small increase in baroreflex control of MAP, but baroreflex control of RSNA was not affected. The results suggest that LPBN neurons have little tonic influence over baroreflex control of MAP and RSNA in the anesthetized rat. When the LPBN is activated, however, LPBN neurons may function to reduce the capacity of the baroreflex to regulate sympathetically mediated increases in arterial pressure.

Dynamic interactions between arterial pressure and sympathetic nerve activity: role of arterial baroreceptors

2003 ◽  
Vol 285 (4) ◽  
pp. R834-R841 ◽  
Author(s):  
Claude Julien ◽  
Bruno Chapuis ◽  
Yong Cheng ◽  
Christian Barrès
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Noise Sources ◽  
Nerve Activity ◽  
Pass Filter ◽  
Low Pass Filter ◽  
Mayer Waves ◽  
Arterial Baroreceptors

The role of arterial baroreceptors in controlling arterial pressure (AP) variability through changes in sympathetic nerve activity was examined in conscious rats. AP and renal sympathetic nerve activity (RSNA) were measured continuously during 1-h periods in freely behaving rats that had been subjected to sinoaortic baroreceptor denervation (SAD) or a sham operation 2 wk before study ( n = 10 in each group). Fast Fourier transform analysis revealed that chronic SAD did not alter high-frequency (0.75-5 Hz) respiratory-related oscillations of mean AP (MAP) and RSNA, decreased by ∼50% spectral power of both variables in the midfrequency band (MF, 0.27-0.74 Hz) containing the so-called Mayer waves, and induced an eightfold increase in MAP power without altering RSNA power in the low-frequency band (0.005-0.27 Hz). In both groups of rats, coherence between RSNA and MAP was maximal in the MF band and was usually weak at lower frequencies. In SAD rats, the transfer function from RSNA to MAP showed the characteristics of a second-order low-pass filter containing a fixed time delay (∼0.5 s). These results indicate that arterial baroreceptors are not involved in production of respiratory-related oscillations of RSNA but play a major role in the genesis of synchronous oscillations of MAP and RSNA at the frequency of Mayer waves. The weak coupling between slow fluctuations of RSNA and MAP in sham-operated and SAD rats points to the interference of noise sources unrelated to RSNA affecting MAP and of noise sources unrelated to MAP affecting RSNA.

Contrasting effects of vasopressin on baroreflex inhibition of lumbar sympathetic nerve activity

1985 ◽  
Vol 249 (5) ◽  
pp. H922-H928 ◽  
Author(s):  
F. M. Sharabi ◽  
G. B. Guo ◽  
F. M. Abboud ◽  
M. D. Thames ◽  
P. G. Schmid
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Sprague Dawley ◽  
Nerve Activity ◽  
Urinary Osmolality ◽  
Arterial Baroreceptors ◽  
Sprague Dawley Rats ◽  
The Difference ◽  
High Level

Baroreflex inhibition of lumbar sympathetic nerve activity (LSNA) during intravenous infusions of phenylephrine and vasopressin is contrasted in rats and rabbits. In rabbits, vasopressin caused smaller increases in arterial pressure and greater inhibition of LSNA than phenylephrine. In Sprague-Dawley rats, however, both vasopressin and phenylephrine caused equivalent increases in arterial pressure and reflex reductions in LSNA. The inhibition of LSNA was mediated through the arterial baroreceptors in both species because it was abolished by sinoaortic denervation. In rats, the possibility that a high level of endogenous vasopressin may have prevented the demonstration of a facilitated baroreflex with the infusion of exogenous vasopressin is unlikely since vasopressin also did not facilitate the reflex in Brattleboro rats, which lack circulating vasopressin. Further, Sprague-Dawley rats were responsive to exogenous vasopressin since infusion of increasing doses of vasopressin caused significant increases in urinary osmolality as well as progressive increments in arterial pressure. The results indicate that intravenous vasopressin given for a period of 6 min facilitates the reflex inhibition of LSNA mediated through arterial baroreceptors in rabbits, but not in rats. Vasopressin given for a period of up to 45 min to rats also fails to facilitate baroreflexes, emphasizing the difference from rabbits. In rabbits, this facilitation appears to involve a central mechanism.

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

2010 ◽  
Vol 299 (4) ◽  
pp. R1114-R1120 ◽  
Author(s):  
Misa Yoshimoto ◽  
Keiko Nagata ◽  
Kenju Miki
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Cardiovascular Function ◽  
Freezing Behavior ◽  
Nerve Activity ◽  
Conscious Rats ◽  
Arterial Baroreceptors

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.

scholarly journals Hypothalamic mTORC1 Signaling Controls Sympathetic Nerve Activity and Arterial Pressure and Mediates Leptin Effects

2013 ◽  
Vol 17 (4) ◽  
pp. 599-606 ◽  
Author(s):  
Shannon M. Harlan ◽  
Deng-Fu Guo ◽  
Donald A. Morgan ◽  
Caroline Fernandes-Santos ◽  
Kamal Rahmouni
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Mtorc1 Signaling

scholarly journals Postexercise hypotension is mediated by reductions in sympathetic nerve activity

1999 ◽  
Vol 276 (1) ◽  
pp. H27-H32 ◽  
Author(s):  
Jennifer M. Kulics ◽  
Heidi L. Collins ◽  
Stephen E. DiCarlo
Keyword(s):  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Peripheral Resistance ◽  
Dynamic Exercise ◽  
Nerve Activity ◽  
Spontaneously Hypertensive ◽  
Before And After ◽  
Postexercise Hypotension ◽  
Carotid Arterial

Mean arterial pressure (MAP), the product of cardiac output (CO) and total peripheral resistance (TPR), is reduced below preexercise levels after a single bout of mild to moderate dynamic exercise. Thus acute, dynamic exercise may be used as a safe, therapeutic approach to reduce MAP. However, the mechanisms responsible for the postexercise hypotension (PEH) are unknown. We tested the hypothesis that PEH is associated with reductions in TPR and sympathetic nerve activity (SNA). Two experimental protocols were designed to test this hypothesis in male spontaneously hypertensive rats (SHR). In protocol 1( n = 9), CO and TPR were determined before, during, and after exercise. In protocol 2 ( n = 7), lumbar SNA (LSNA) was recorded before and after exercise. Rats in protocol 1 were chronically instrumented with left carotid arterial catheters and ascending aortic Doppler ultrasonic flow probes. Rats in protocol 2 were chronically instrumented with left carotid arterial catheters and electrodes around the lumbar sympathetic trunk. Dynamic treadmill exercise (9–12 m/min, 10% grade for 40 min) resulted in a postexercise reduction in MAP (from 143 ± 5 to 128 ± 4 mmHg, P < 0.05). Associated with the PEH was a reduction in TPR (from 28 ± 3 to 19 ± 2 mmHg/kHz; P < 0.05) and an elevation in CO (from 5.7 ± 0.4 to 7.2 ± 0.5 kHz; P < 0.05). The reductions in arterial pressure and TPR were associated with a decrease in LSNA (from 98 ± 3 to 49 ± 6%; P < 0.05). These results suggest that PEH is mediated by reductions in TPR and SNA.

Cerebral sympathetic nerve activity has a major regulatory role in the cerebral circulation in REM sleep

2009 ◽  
Vol 106 (4) ◽  
pp. 1050-1056 ◽  
Author(s):  
Priscila A. Cassaglia ◽  
Robert I. Griffiths ◽  
Adrian M. Walker
Keyword(s):  
Arterial Pressure ◽  
Blood Vessels ◽  
Rem Sleep ◽  
Sympathetic Nerve ◽  
Cerebral Circulation ◽  
Sympathetic Nerve Activity ◽  
Nrem Sleep ◽  
Protective Mechanism ◽  
Nerve Activity ◽  
Phasic Rem Sleep

Sympathetic nerve activity (SNA) in neurons projecting to skeletal muscle blood vessels increases during rapid-eye-movement (REM) sleep, substantially exceeding SNA of non-REM (NREM) sleep and quiet wakefulness (QW). Similar SNA increases to cerebral blood vessels may regulate the cerebral circulation in REM sleep, but this is unknown. We hypothesized that cerebral SNA increases during phasic REM sleep, constricting cerebral vessels as a protective mechanism against cerebral hyperperfusion during the large arterial pressure surges that characterize this sleep state. We tested this hypothesis using a newly developed model to continuously record SNA in the superior cervical ganglion (SCG) before, during, and after arterial pressure surges occurring during REM in spontaneously sleeping lambs. Arterial pressure (AP), intracranial pressure (ICP), cerebral blood flow (CBF), cerebral vascular resistance [CVR = (AP − ICP)/CBF], and SNA from the SCG were recorded in lambs ( n = 5) undergoing spontaneous sleep-wake cycles. In REM sleep, CBF was greatest (REM > QW = NREM, P < 0.05) and CVR was least (REM < QW = NREM, P < 0.05). SNA in the SCG did not change from QW to NREM sleep but increased during tonic REM sleep, with a further increase during phasic REM sleep (phasic REM > tonic REM > QW = NREM, P < 0.05). Coherent averaging revealed that SNA increases preceded AP surges in phasic REM sleep by 12 s ( P < 0.05). We report the first recordings of cerebral SNA during natural sleep-wake cycles. SNA increases markedly during tonic REM sleep, and further in phasic REM sleep. As SNA increases precede AP surges, they may serve to protect the brain against potentially damaging intravascular pressure changes or hyperperfusion in REM sleep.

scholarly journals Adrenomedullin increases cardiac sympathetic nerve activity in normal conscious sheep

2005 ◽  
Vol 187 (2) ◽  
pp. 275-281 ◽  
Author(s):  
C J Charles ◽  
D L Jardine ◽  
M G Nicholls ◽  
A M Richards
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Vehicle Control ◽  
Cardiac Sympathetic Nerve ◽  
Burst Frequency ◽  
Nerve Activity ◽  
Cardiac Sympathetic Nerve Activity ◽  
Conscious Sheep

The sympathetic nervous system and adrenomedullin (AM) both participate in the regulation of cardiac and circulatory function but their interaction remains uncertain. We have examined the effects of AM on cardiac sympathetic nerve activity (CSNA) and hemodynamics and contrasted these effects with pressure-matched nitro-prusside (NP) administration in normal conscious sheep. Compared with vehicle control, arterial pressure fell similarly with AM (P=0.04) and NP (P<0.001). Heart rate rose in response to both AM (P<0.001) and NP (P=0.002) but the rise with AM was significantly greater than that induced by NP (P<0.001). Cardiac output increased in response to AM compared with both control and NP (both P<0.001). CSNA burst frequency (bursts/min) were increased in response to both AM (P<0.001) and NP (P=0.005) with the rise in burst frequency being greater with AM compared with NP (P<0.001). CSNA burst area/min was also raised by both AM (P=0.03) and NP (P=0.002) with a trend for burst area being greater with AM than NP (P=0.07). CSNA burst incidence (bursts/100 beats) showed no significant differences between any treatment day. In conclusion, we have demonstrated that AM is associated with a greater increase in CSNA and heart rate for a given change in arterial pressure than seen with the classic balanced vasodilator NP.

Measurement of sympathetic nerve activity in the unanesthetized rat

1989 ◽  
Vol 67 (1) ◽  
pp. 250-255 ◽  
Author(s):  
J. P. Fluckiger ◽  
G. Gremaud ◽  
B. Waeber ◽  
A. Kulik ◽  
A. Ichino ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Blood Pressure Reduction ◽  
Response Curves ◽  
Nerve Activity ◽  
Dose Dependent

A new system was developed in our laboratory to continuously monitor intra-arterial pressure, heart rate, and sympathetic nerve activity in unanesthetized rats. The animals were prepared 24 h before the start of the experiments. Sympathoneural traffic was measured at the level of splanchnic nerve. The amplitude of the spikes recorded at this level was utilized to express sympathetic nerve activity. The amplitude of the residual electroneurogram signal present 30 min after the rats were killed was 32 +/- 2 mV (mean +/- SE; n = 11). For analysis, these background values were subtracted from values determined in vivo. The nerve we studied contains postganglionic fibers, since electrical activity decreased in response to ganglionic blockade with pentolinium (1.25 mg/min iv for 4 min). The amplitude of spikes fell by 43 +/- 4% (n = 4). Sympathetic nerve activity was highly reproducible at a 24-h interval (104 +/- 26 vs. 111 +/- 27 mV for the amplitude of spikes; n = 11). Dose-response curves to the alpha 1-stimulant methoxamine and to bradykinin were established in four rats. The increase in blood pressure induced by methoxamine caused a dose-dependent fall in sympathetic nerve activity, whereas the blood pressure reduction resulting from bradykinin was associated with a dose-dependent activation of sympathetic drive. These data therefore indicate that it is possible with out system to accurately measure sympathetic nerve activity in the awake rat, together with intra-arterial pressure and heart rate.

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