Document Detail


Endothelium-dependent cerebral artery dilation mediated by transient receptor potential and Ca2+-activated K+ channels.
MedLine Citation:
PMID:  20729757     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Intracellular Ca(2+) plays a dual role in the regulation of vascular tone. Smooth muscle cell Ca(2+) influx causes vasoconstriction, whereas transient localized Ca(2+) release from intracellular stores in either endothelial or vascular smooth muscle cells can elicit membrane hyperpolarization and vasodilation by stimulating Ca(2+)-activated K(+) (K(Ca)) channels. Recent evidence suggests that Ca(2+) influx via transient receptor potential (TRP) channels can cause arterial dilation by activating K(Ca) channels. Current findings in this area are summarized. Key features of the main KCa channels present in the vascular wall (K(Ca)1.1, K(Ca)2.3, and K(Ca)3.1) and TRP channels are briefly reviewed. Arterial dilation mediated by endothelial TRP channels sensitive to dietary molecules are reviewed. Recent reports demonstrate that 2 chemosensitive TRP channels, TRPA1 and TRPV3, are present in native cerebral artery endothelial cells. These channels are activated by substances found in foods such as garlic, mustard oil, and oregano and mediate K(Ca)-dependent endothelium-dependent vasodilation. The role of TRPV4 channels in mediating vasodilation in response to epoxyeicosatrienoic acids (EETs) is also reviewed. Stimulation of TRPV4 channels with 11,12-EET in cerebral artery smooth muscle cells causes membrane hyperpolarization and vasodilation by increasing the frequency of Ca(2+) release from intracellular stores, which in turn increases K(Ca)1.1 channel activity. Evidence that K(Ca)2.3 and K(Ca)3.1 channels in endothelial cells and K(Ca)1.1 channels in smooth muscle are involved in TRPV4-dependent 11,12-EET–induced dilation of mesenteric arteries is discussed. These examples show that Ca(2+) influx through TRP channels in endothelial or smooth muscle cells influences vascular tone by increasing K(Ca) channel activity.
Authors:
Scott Earley
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Review    
Journal Detail:
Title:  Journal of cardiovascular pharmacology     Volume:  57     ISSN:  1533-4023     ISO Abbreviation:  J. Cardiovasc. Pharmacol.     Publication Date:  2011 Feb 
Date Detail:
Created Date:  2011-05-02     Completed Date:  2012-02-27     Revised Date:  2014-09-19    
Medline Journal Info:
Nlm Unique ID:  7902492     Medline TA:  J Cardiovasc Pharmacol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  148-53     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Cerebral Arteries / drug effects,  physiology*
Endothelium, Vascular / drug effects,  metabolism,  physiology*
Humans
Muscle, Smooth, Vascular / drug effects,  metabolism,  physiology
Potassium Channels, Calcium-Activated / physiology*
TRPV Cation Channels / physiology
Transient Receptor Potential Channels / physiology*
Grant Support
ID/Acronym/Agency:
R01 HL091905/HL/NHLBI NIH HHS; R01HL091905/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Potassium Channels, Calcium-Activated; 0/TRPV Cation Channels; 0/TRPV4 protein, human; 0/Transient Receptor Potential Channels

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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