Trophic effect of the sympathetic nervous system on vascular smooth muscle

1983 ◽  
Vol 11 (6) ◽  
pp. 607-615 ◽  
Author(s):  
K. Fronek
Keyword(s):  
Nervous System ◽  
Smooth Muscle ◽  
Sympathetic Nervous System ◽  
Vascular Smooth Muscle ◽  
Trophic Effect ◽  
Sympathetic Nervous

General Anesthetics and Vascular Smooth Muscle

2007 ◽  
Vol 106 (2) ◽  
pp. 365-391 ◽  
Author(s):  
Takashi Akata ◽  
David C. Warltier
Keyword(s):  
Nervous System ◽  
Smooth Muscle ◽  
Sympathetic Nervous System ◽  
Vascular Smooth Muscle ◽  
Vascular Resistance ◽  
Cardiovascular Reflexes ◽  
Organ Blood Flow ◽  
General Anesthetics ◽  
Sympathetic Nervous

General anesthetics threaten cardiovascular stability by causing changes in cardiac function, vascular reactivity, and cardiovascular reflexes and significantly alter distribution of cardiac output to various organs. Their overall impact is often systemic hypotension, which is attributable to myocardial depression, peripheral vasodilation, and attenuated sympathetic nervous system activity. However, one could be more causative than the others, depending on anesthetic agents and cardiovascular factors inherent in patients (e.g., coexisting heart disease). It is generally believed that most general anesthetics attenuate sympathetic nervous system outflow from the central nervous system, thereby decreasing vascular resistance in peripheral circulations. Indeed, in previous in vivo studies, during administration of various general anesthetics, vascular resistance was decreased in most peripheral circulations; however, it was unaffected or increased in some peripheral circulations. General anesthetics may act directly on vascular smooth muscle and/or endothelial cells in various vascular beds, influencing total peripheral and/or regional vascular resistance, and hence organ blood flow. This article reviews previously reported direct (i.e., nonneural) vascular actions of general anesthetics and discusses their underlying mechanisms, their in vivo relevance, and the future of research for general anesthetic vascular pharmacology.

Trophic effect of the sympathetic nervous system on the early development of the rat parotid gland: A quantitative ultrastructural study

1981 ◽  
Vol 201 (4) ◽  
pp. 645-654 ◽  
Author(s):  
Gunnar D. Bloom ◽  
Bengt Carlsöö ◽  
Åke Danielsson ◽  
Sten Hellström ◽  
Roger Henriksson
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Parotid Gland ◽  
Early Development ◽  
Ultrastructural Study ◽  
Trophic Effect ◽  
Rat Parotid Gland ◽  
Sympathetic Nervous ◽  
Rat Parotid

Influences of exogenous insulin on arterial blood pressure measurements of the rat

1989 ◽  
Vol 67 (6) ◽  
pp. 2335-2342 ◽  
Author(s):  
J. G. Edwards ◽  
C. M. Tipton
Keyword(s):  
Blood Pressure ◽  
Nervous System ◽  
Smooth Muscle ◽  
Sympathetic Nervous System ◽  
Arterial Blood Pressure ◽  
Insulin Infusion ◽  
Control Period ◽  
Male Rats ◽  
Arterial Blood ◽  
Sympathetic Nervous

Studies were undertaken with adult male rats to test the hypothesis that euglycemic hyperinsulinemia would alter mean arterial blood pressure (MAP) and heart rate (HR) relationships by activation of the sympathetic nervous system. Conscious rats were infused either with insulin or control vehicle (0, 0.47, 1.5, 4.7, 15.0 mU.kg-1.min-1) for 75 min before injection of hexamethonium. Compared with the control period, insulin infusion significantly increased MAP by 7.1 +/- 0.1, 12.7 +/- 2.0, and 19.7 +/- 0.3 (SE) mmHg and HR by 44 +/- 8.4, 66 +/- 10.3, and 95 +/- 6.3 beats/min, respectively, during the three highest rates of infusion. The dose-dependent increases in MAP and HR were due to increases in the activity of hexamethonium-sensitive pathways. In chemically sympathectomized rats, insulin infusion did not produce a significant increase in either MAP or HR. The influence of exogenous norepinephrine on MAP and HR was also studied after insulin infusion. Compared with the insulin-vehicle infusion, insulin infusion significantly depressed (P less than 0.05) the norepinephrine dose-response increase in MAP. In addition, isolated smooth muscle strips were studied to determine the influence of insulin on their in vitro responses to increasing doses of norepinephrine. Although insulin did not alter contractility, it significantly (P less than 0.05) decreased the sensitivity of the vascular strips to norepinephrine. Collectively, the data from these euglycemic experiments indicated that infusions of insulin caused increases in HR and MAP because of activation of the sympathetic nervous system, even though the responsiveness of the vascular smooth muscle was depressed.

The Trophic Effect of the Sympathetic Nervous System on Cells of the Septal Region of the Basal Forebrain

1993 ◽  
Vol 8 (1) ◽  
pp. 35-39
Author(s):  
Ewa Chelmicka-schorr ◽  
Michael N. Kwasniewski ◽  
David N. Hammond
Keyword(s):  
Nervous System ◽  
Sympathetic Nervous System ◽  
Basal Forebrain ◽  
Trophic Effect ◽  
Septal Region ◽  
Sympathetic Nervous
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