Endothelial-smooth muscle cell interactions in the regulation of vascular tone in skeletal muscle.

The smooth muscle cells (SMCs) of skeletal muscle arterioles are intricately sensitive to changes in membrane potential. Upon increasing luminal pressure, the SMCs depolarize, thereby opening voltage-dependent Ca(2+) channels (VDCCs), which leads to contraction. Mechanisms that oppose this myogenic...

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Main Author: Dora, K
Format: Journal article
Language:English
Published: Wiley 2016
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author Dora, K
author_facet Dora, K
author_sort Dora, K
collection OXFORD
description The smooth muscle cells (SMCs) of skeletal muscle arterioles are intricately sensitive to changes in membrane potential. Upon increasing luminal pressure, the SMCs depolarize, thereby opening voltage-dependent Ca(2+) channels (VDCCs), which leads to contraction. Mechanisms that oppose this myogenic tone can involve voltage-dependent and independent dilator pathways, and can be endothelium-dependent or independent. Of particular interest are the pathways leading to hyperpolarization of SMCs, as these can potentially evoke both local and conducted dilation. This review focuses on three agonists that cause local and conducted dilation in skeletal muscle: acetylcholine (ACh), adenosine triphosphate (ATP) and KCl. The mechanisms for the release of these agonists during motor nerve stimulation and/or hypoxia, and their actions to open either Ca(2+) -activated K(+) channels (KC a ) or inwardly rectifying K(+) channels (KIR ) are described. By causing local and conducted dilation, each agonist has the ability to improve skeletal muscle blood flow during exercise and ischemia. This article is protected by copyright. All rights reserved.
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spelling oxford-uuid:b2cd5026-5d33-4979-9fed-89654bee63652022-03-27T04:14:16ZEndothelial-smooth muscle cell interactions in the regulation of vascular tone in skeletal muscle.Journal articlehttp://purl.org/coar/resource_type/c_dcae04bcuuid:b2cd5026-5d33-4979-9fed-89654bee6365EnglishSymplectic Elements at OxfordWiley2016Dora, KThe smooth muscle cells (SMCs) of skeletal muscle arterioles are intricately sensitive to changes in membrane potential. Upon increasing luminal pressure, the SMCs depolarize, thereby opening voltage-dependent Ca(2+) channels (VDCCs), which leads to contraction. Mechanisms that oppose this myogenic tone can involve voltage-dependent and independent dilator pathways, and can be endothelium-dependent or independent. Of particular interest are the pathways leading to hyperpolarization of SMCs, as these can potentially evoke both local and conducted dilation. This review focuses on three agonists that cause local and conducted dilation in skeletal muscle: acetylcholine (ACh), adenosine triphosphate (ATP) and KCl. The mechanisms for the release of these agonists during motor nerve stimulation and/or hypoxia, and their actions to open either Ca(2+) -activated K(+) channels (KC a ) or inwardly rectifying K(+) channels (KIR ) are described. By causing local and conducted dilation, each agonist has the ability to improve skeletal muscle blood flow during exercise and ischemia. This article is protected by copyright. All rights reserved.
spellingShingle Dora, K
Endothelial-smooth muscle cell interactions in the regulation of vascular tone in skeletal muscle.
title Endothelial-smooth muscle cell interactions in the regulation of vascular tone in skeletal muscle.
title_full Endothelial-smooth muscle cell interactions in the regulation of vascular tone in skeletal muscle.
title_fullStr Endothelial-smooth muscle cell interactions in the regulation of vascular tone in skeletal muscle.
title_full_unstemmed Endothelial-smooth muscle cell interactions in the regulation of vascular tone in skeletal muscle.
title_short Endothelial-smooth muscle cell interactions in the regulation of vascular tone in skeletal muscle.
title_sort endothelial smooth muscle cell interactions in the regulation of vascular tone in skeletal muscle
work_keys_str_mv AT dorak endothelialsmoothmusclecellinteractionsintheregulationofvasculartoneinskeletalmuscle