Blood pressure control and the peripheral sympathetic nervous system

1984 ◽  
pp. 24-33
Author(s):  
C. J. Mathias
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blood Pressure Control ◽  
Pressure Control ◽  
Sympathetic Nervous ◽  
Peripheral Sympathetic Nervous System

Interactions between ANG II, sympathetic nervous system, and baroreceptor reflexes in regulation of blood pressure

1992 ◽  
Vol 262 (6) ◽  
pp. E763-E778 ◽  
Author(s):  
I. A. Reid
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Blood Pressure Control ◽  
Cardiovascular Responses ◽  
Pressure Control ◽  
Ang Ii ◽  
Arterial Blood ◽  
Baroreceptor Reflexes ◽  
Sympathetic Nervous

The renin-angiotensin system plays an important role in the regulation of arterial blood pressure and in the development of some forms of clinical and experimental hypertension. It is an important blood pressure control system in its own right but also interacts extensively with other blood pressure control systems, including the sympathetic nervous system and the baroreceptor reflexes. Angiotensin (ANG) II exerts several actions on the sympathetic nervous system. These include a central action to increase sympathetic outflow, stimulatory effects on sympathetic ganglia and the adrenal medulla, and actions at sympathetic nerve endings that serve to facilitate sympathetic neurotransmission. ANG II also interacts with baroreceptor reflexes. For example, it acts centrally to modulate the baroreflex control of heart rate, and this accounts for its ability to increase blood pressure without causing a reflex bradycardia. The physiological significance of these actions of ANG II is not fully understood. Most evidence indicates that the actions of ANG to enhance sympathetic activity do not contribute significantly to the pressor response to exogenous ANG II. On the other hand, there is considerable evidence that the actions of endogenous ANG II on the sympathetic nervous system enhance the cardiovascular responses elicited by activation of the sympathetic nervous system.

scholarly journals Central actions of circulating angiotensin II on the sympathetic nervous system and blood pressure control.

1985 ◽  
Vol 26 (1) ◽  
pp. 105-112 ◽  
Author(s):  
Yuji UENO ◽  
Mikio ARITA ◽  
Hidetoshi SURUDA ◽  
Osamu MOHARA ◽  
Yoshiaki MASUYAMA ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Angiotensin Ii ◽  
Sympathetic Nervous System ◽  
Blood Pressure Control ◽  
Pressure Control ◽  
Central Actions ◽  
Sympathetic Nervous

Abstract MP07: Endogenous Chemerin Amplifies Nerve-Dependent Arterial Contraction

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Emma Darios ◽  
Stephanie W Watts
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Superior Mesenteric Artery ◽  
Mesenteric Artery ◽  
Sympathetic Innervation ◽  
Pressure Control ◽  
Perivascular Adipose Tissue ◽  
Sympathetic Nervous ◽  
Isolated Arteries

The adipokine chemerin causes contraction of isolated arteries and is implicated in blood pressure regulation, especially in the obese population that have elevated levels of circulating chemerin. Because chemerin is expressed in the perivascular adipose tissue (PVAT) that facilitates the sympathetic innervation of the blood vessel, we tested the hypothesis that chemerin (endogenous and exogenous) would amplify the effects of the sympathetic nervous system in mediating electrical field stimulated (EFS) contraction. The model was the superior mesenteric artery with PVAT, mounted into tissue baths for isometric contraction. Immunohistochemistry validated a robust expression of chemerin in the PVAT surrounding the superior mesenteric artery. EFS (0.3-20 Hz) caused a frequency-dependent, prazosin-sensitive contraction that was reduced (~40%) by the chemerin receptor ChemR23 antagonist CCX832 (100 nM; figure) but not by the inactive congener CCX826 (100 nM). Exogenous chemerin (1 μM) amplified EFS-induced contraction in a manner that was also blocked by CCX832. Chemerin did not directly modify contraction of the superior mesenteric artery (-PVAT) to cumulative concentrations of norepinephrine (1 nM - 10 μM), supporting that contractile amplification by chemerin was not at the level of smooth muscle. These studies raise the interesting possibilities that endogenous chemerin and/or ChemR23 modifies nerve-mediated contraction. This is significant because of the well appreciated role of the sympathetic nervous system in blood pressure control.

Acute elevation of plasma non-esterified fatty acids increases pulse wave velocity and induces peripheral vasodilation in humans in vivo

2007 ◽  
Vol 113 (1) ◽  
pp. 33-40 ◽  
Author(s):  
Niels P. Riksen ◽  
Marlies Bosselaar ◽  
Stephan J.L. Bakker ◽  
Robert J. Heine ◽  
Gerard A. Rongen ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Sympathetic Nervous System ◽  
Pulse Wave Velocity ◽  
Wave Velocity ◽  
Adenosine Receptor ◽  
Pulse Wave ◽  
Adenosine Receptor Antagonist ◽  
Sympathetic Nervous ◽  
Control Infusion

Plasma NEFA (non-esterified fatty acid) concentrations are elevated in patients with obesity. In the present study we first aimed to provide an integral haemodynamic profile of elevated plasma NEFAs by the simultaneous assessment of blood pressure, pulse wave velocity, FBF (forearm blood flow) and sympathetic nervous system activity during acute elevation of NEFAs. Secondly, we hypothesized that NEFA-induced vasodilation is mediated by adenosine receptor stimulation. In a randomized cross-over trial in healthy subjects, Intralipid® was infused for 2 h to elevate plasma NEFAs. Glycerol was administered as the Control infusion. We assessed blood pressure, pulse wave velocity, FBF (using venous occlusion plethysmography) and sympathetic nervous system activity by measurement of noradrenaline and adrenaline. During the last 15 min of Intralipid®/Control infusion, the adenosine receptor antagonist caffeine (90 μg·min−1·dl−1) was administered into the brachial artery of the non-dominant arm. Compared with Control infusion, Intralipid® increased pulse wave velocity, SBP (systolic blood pressure) and pulse pressure, as well as FBF (from 1.8±0.2 to 2.7±0.6 and from 2.3±0.2 to 2.7±0.6 ml·min−1·dl−1 for Intralipid® compared with Control infusion; P<0.05, n=9). Although in a positive control study caffeine attenuated adenosine-induced forearm vasodilation (P<0.01, n=6), caffeine had no effect on Intralipid®-induced vasodilation (P=0.5). In conclusion, elevation of plasma NEFA levels increased pulse wave velocity, SBP and pulse pressure. FBF was also increased, either by baroreflex-mediated inhibition of the sympathetic nervous system or by a direct vasodilating effect of NEFAs. As the adenosine receptor antagonist caffeine could not antagonize the vasodilator response, this response is not mediated by adenosine receptor stimulation.

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