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Endothelial Ca(2+) signaling-dependent vasodilation through transient receptor potential channels

Ca(2+) signaling of endothelial cells plays a critical role in controlling blood flow and pressure in small arteries and arterioles. As the impairment of endothelial function is closely associated with cardiovascular diseases (e.g., atherosclerosis, stroke, and hypertension), endothelial Ca(2+) sign...

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Autores principales: Hong, Kwang-Seok, Lee, Man-Gyoon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: The Korean Physiological Society and The Korean Society of Pharmacology 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7317173/
https://www.ncbi.nlm.nih.gov/pubmed/32587123
http://dx.doi.org/10.4196/kjpp.2020.24.4.287
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author Hong, Kwang-Seok
Lee, Man-Gyoon
author_facet Hong, Kwang-Seok
Lee, Man-Gyoon
author_sort Hong, Kwang-Seok
collection PubMed
description Ca(2+) signaling of endothelial cells plays a critical role in controlling blood flow and pressure in small arteries and arterioles. As the impairment of endothelial function is closely associated with cardiovascular diseases (e.g., atherosclerosis, stroke, and hypertension), endothelial Ca(2+) signaling mechanisms have received substantial attention. Increases in endothelial intracellular Ca(2+) concentrations promote the synthesis and release of endothelial-derived hyperpolarizing factors (EDHFs, e.g., nitric oxide, prostacyclin, or K(+) efflux) or directly result in endothelial-dependent hyperpolarization (EDH). These physiological alterations modulate vascular contractility and cause marked vasodilation in resistance arteries. Transient receptor potential (TRP) channels are nonselective cation channels that are present in the endothelium, vascular smooth muscle cells, or perivascular/sensory nerves. TRP channels are activated by diverse stimuli and are considered key biological apparatuses for the Ca(2+) influx-dependent regulation of vasomotor reactivity in resistance arteries. Ca(2+)-permeable TRP channels, which are primarily found at spatially restricted microdomains in endothelial cells (e.g., myoendothelial projections), have a large unitary or binary conductance and contribute to EDHFs or EDH-induced vasodilation in concert with the activation of intermediate/small conductance Ca(2+)-sensitive K(+) channels. It is likely that endothelial TRP channel dysfunction is related to the dysregulation of endothelial Ca(2+) signaling and in turn gives rise to vascular-related diseases such as hypertension. Thus, investigations on the role of Ca(2+) dynamics via TRP channels in endothelial cells are required to further comprehend how vascular tone or perfusion pressure are regulated in normal and pathophysiological conditions.
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spelling pubmed-73171732020-07-01 Endothelial Ca(2+) signaling-dependent vasodilation through transient receptor potential channels Hong, Kwang-Seok Lee, Man-Gyoon Korean J Physiol Pharmacol Review Article Ca(2+) signaling of endothelial cells plays a critical role in controlling blood flow and pressure in small arteries and arterioles. As the impairment of endothelial function is closely associated with cardiovascular diseases (e.g., atherosclerosis, stroke, and hypertension), endothelial Ca(2+) signaling mechanisms have received substantial attention. Increases in endothelial intracellular Ca(2+) concentrations promote the synthesis and release of endothelial-derived hyperpolarizing factors (EDHFs, e.g., nitric oxide, prostacyclin, or K(+) efflux) or directly result in endothelial-dependent hyperpolarization (EDH). These physiological alterations modulate vascular contractility and cause marked vasodilation in resistance arteries. Transient receptor potential (TRP) channels are nonselective cation channels that are present in the endothelium, vascular smooth muscle cells, or perivascular/sensory nerves. TRP channels are activated by diverse stimuli and are considered key biological apparatuses for the Ca(2+) influx-dependent regulation of vasomotor reactivity in resistance arteries. Ca(2+)-permeable TRP channels, which are primarily found at spatially restricted microdomains in endothelial cells (e.g., myoendothelial projections), have a large unitary or binary conductance and contribute to EDHFs or EDH-induced vasodilation in concert with the activation of intermediate/small conductance Ca(2+)-sensitive K(+) channels. It is likely that endothelial TRP channel dysfunction is related to the dysregulation of endothelial Ca(2+) signaling and in turn gives rise to vascular-related diseases such as hypertension. Thus, investigations on the role of Ca(2+) dynamics via TRP channels in endothelial cells are required to further comprehend how vascular tone or perfusion pressure are regulated in normal and pathophysiological conditions. The Korean Physiological Society and The Korean Society of Pharmacology 2020-07-01 2020-07-01 /pmc/articles/PMC7317173/ /pubmed/32587123 http://dx.doi.org/10.4196/kjpp.2020.24.4.287 Text en Copyright © Korean J Physiol Pharmacol This is an open-access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/4.0) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Review Article
Hong, Kwang-Seok
Lee, Man-Gyoon
Endothelial Ca(2+) signaling-dependent vasodilation through transient receptor potential channels
title Endothelial Ca(2+) signaling-dependent vasodilation through transient receptor potential channels
title_full Endothelial Ca(2+) signaling-dependent vasodilation through transient receptor potential channels
title_fullStr Endothelial Ca(2+) signaling-dependent vasodilation through transient receptor potential channels
title_full_unstemmed Endothelial Ca(2+) signaling-dependent vasodilation through transient receptor potential channels
title_short Endothelial Ca(2+) signaling-dependent vasodilation through transient receptor potential channels
title_sort endothelial ca(2+) signaling-dependent vasodilation through transient receptor potential channels
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7317173/
https://www.ncbi.nlm.nih.gov/pubmed/32587123
http://dx.doi.org/10.4196/kjpp.2020.24.4.287
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