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Vascular KCNQ channels in humans: the sub‐threshold brake that regulates vascular tone?
Author(s) -
Mani Bharath K.,
Byron Kenneth L.
Publication year - 2011
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.2010.01065.x
Subject(s) - contractility , vascular smooth muscle , vasoconstriction , contraction (grammar) , potassium channel , pinacidil , ion channel , muscle contraction , voltage dependent calcium channel , membrane potential , chemistry , neuroscience , calcium , biology , medicine , endocrinology , smooth muscle , receptor , glibenclamide , diabetes mellitus
Contraction of arterial smooth muscle cells results in vasoconstriction, which in turn reduces blood flow and increases blood pressure. There has been a great deal of interest in understanding the ionic mechanisms that regulate smooth muscle contraction, in part because ion channels represent potential pharmacological targets for therapies directed towards cardiovascular diseases and other conditions. Potassium channels have been recognized for their roles in maintaining or stabilizing negative membrane voltages. Activation of potassium channels opposes opening of voltage-sensitive calcium channels which conduct calcium ions into the smooth muscle cells to stimulate contraction. KCNQ potassium channels were recently discovered in arterial smooth muscle cells from rats and mice. These channels have distinctive pharmacological and biophysical characteristics that have led them to be implicated as important regulators of membrane voltage and as novel pharmacological targets for modulation of vascular contractility. In this issue of British Journal of Pharmacology, Ng et al., extend the findings from rodent models to the human vasculature and establish that KCNQ channels also regulate constriction of human arteries. The findings have important implications for the use of pharmacological KCNQ channel modulators to treat human diseases.