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T‐type calcium channels and vascular function: the new kid on the block?
Author(s) -
Kuo Ivana Y.T.,
Wölfle Stephanie E.,
Hill Caryl E.
Publication year - 2011
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2010.199497
Subject(s) - voltage dependent calcium channel , l type calcium channel , calcium channel , t type calcium channel , vasoconstriction , r type calcium channel , downregulation and upregulation , vascular smooth muscle , microbiology and biotechnology , calcium , n type calcium channel , chemistry , medicine , endocrinology , neuroscience , biology , biochemistry , smooth muscle , gene
While L‐type voltage‐dependent calcium channels have long been considered the predominant source of calcium for myogenic constriction, recent studies of both cerebral and systemic circulations have provided evidence for the prominent expression of other members of the voltage‐dependent calcium channel family, in particular the low voltage activated T‐type channels. Although physiological studies have not supported the involvement of a classical low voltage activated, T‐type channel in vascular function, evidence is accumulating that points to the involvement of a non‐L‐type, high voltage activated channel with sensitivity to T‐type channel antagonists. We propose that this may arise due to expression of a T‐type channel splice variant with unique biophysical characteristics resulting in a more depolarised profile. Expression of these channels in smooth muscle cells would broaden the voltage range over which sustained calcium influx occurs, while expression of T‐type channels in endothelial cells could provide a feedback mechanism to prevent excessive vasoconstriction. Perturbation of this balance during pathophysiological conditions by upregulation of channel expression and endothelial dysfunction could contribute to vasospastic conditions and therapy‐refractory hypertension.