Channelpedia

PubMed 12378818


Referenced in Channelpedia wiki pages of: none

Automatically associated channels: Kv1.2 , Kv1.5 , Slo1



Title: Changes in the expression and function of arterial potassium channels during hypertension.

Authors: Robert H Cox

Journal, date & volume: Vascul. Pharmacol., 2002 Jan , 38, 13-23

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/12378818


Abstract
Altered function of K+ channels associated with hypertension has been inferred from the effects of K+ channel blockers on contraction of arterial smooth muscle cells (SMCs) and from K+ efflux measurements. Of the classes of K+ channels known to exist in the smooth muscle, the contribution of voltage-gated (KV) and high-conductance, Ca2+ gated K+ (BKCa) channels to the regulation of arterial SMC contractile function has been the most studied in hypertension. The effects of selective and nonselective K+ channel blockers on tonic contraction suggest that these two K+ channel gene families contribute differently to total K+ conductance in arterial SMCs from normal and hypertensive subjects. Direct measurements of K+ channel properties by electrophysiological methods generally support this conclusion. Studies have demonstrated larger BKCa currents in SMCs from several arteries of hypertensive rats, which have been reported to result from a greater Ca2+ sensitivity of BKCa channels and/or from greater protein expression. Some, but not all, studies have shown decreased KV currents in arterial SMCs from hypertensive animals measured under Ca(2+)-replete conditions. However, when external Ca2+ is removed or when Ca2+ influx is inhibited, KV currents are larger in SMCs exposed to chronic hypertension. Gene expression studies of Shaker KV1 transcripts have shown that of the dominant species present in arterial SMCs, KV1.2 expression is higher, whereas KV1.5 is the same in SMCs from hypertensive compared to normal animals. This finding is consistent with the larger KV currents in vascular SMCs from hypertensive animals under low Ca2+ conditions and suggests that Ca2+ influx and/or intracellular Ca2+ per se exerts a greater inhibitory effect on KV currents in the myocytes from these animals. The pathways by which these K+ channel differences are produced during hypertension remain to be elucidated, as does the potential for these channel proteins to be targeted by novel antihypertensive therapies.