scholarly journals Arcuate Angiotensin II increases arterial pressure via coordinated increases in sympathetic nerve activity and vasopressin secretion

eNeuro ◽  
2021 ◽  
pp. ENEURO.0404-21.2021
Author(s):  
Zhigang Shi ◽  
Daniel S. Stornetta ◽  
Ruth L. Stornetta ◽  
Virginia L. Brooks
Keyword(s):  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Nerve Activity ◽  
Vasopressin Secretion

Effects of intravenous infusions of angiotensin II on muscle sympathetic nerve activity in humans

1991 ◽  
Vol 261 (3) ◽  
pp. R690-R696 ◽  
Author(s):  
T. Matsukawa ◽  
E. Gotoh ◽  
K. Minamisawa ◽  
M. Kihara ◽  
S. Ueda ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Muscle Sympathetic Nerve Activity ◽  
Sympathetic Outflow ◽  
Ang Ii ◽  
Nerve Activity ◽  
Intravenous Infusions

The effect of angiotensin II (ANG II) on the sympathetic outflow was examined in normal humans. The mean arterial pressure and muscle sympathetic nerve activity (MSNA) were measured before and during intravenous infusions of phenylephrine (0.5 and 1.0 micrograms.kg-1.min-1) or ANG II (5, 10, and 20 ng.kg-1.min-1) for 15 min at 30-min intervals. The baroreflex slope for the relationship between the increases in mean arterial pressure and the reductions in MSNA was significantly less acute during the infusions of ANG II than during the infusions of phenylephrine. When nitroprusside was infused simultaneously to maintain central venous pressure at the basal level, MSNA significantly increased during the infusions of ANG II (5 ng.kg-1.min-1 for 15 min) but not during the infusions of phenylephrine (1.0 micrograms.kg-1.min-1 for 15 min), with accompanying attenuation of the elevation in arterial pressure induced by these pressor agents. These findings suggest that ANG II stimulates the sympathetic outflow without mediating baroreceptor reflexes in humans.

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.

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