PubMed 19537928
Referenced in: none
Automatically associated channels: BKβ
Title: Vasorelaxing action of vasonatrin peptide is associated with activation of large-conductance Ca(2+)-activated potassium channels in vascular smooth muscle cells.
Authors: J Yu, M Zhu, Z Fu, X Zhu, Y Zhao, B Chen
Journal, date & volume: Physiol Res, 2010 , 59, 187-94
PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/19537928
Abstract
The aim of this study was to test the hypothesis that vasorelaxing action of vasonatrin peptide (VNP) is due to activation of the large-conductance Ca(2+)-activated potassium channel (BK(Ca)) via guanylyl cyclase (GC)-coupled natriuretic peptide receptors (NPRs) in vascular smooth muscle cells (VSMCs). Contraction experiments were performed using human radial artery, whereas BK(Ca) current by patch clamp was recorded in cells from rat mesenteric artery. Contractility of rings cut from human radial artery was detected in vitro. As a result, VNP induced a dose-dependent vasorelaxation of human radial artery, which could be mimicked by 8-Br-cGMP, and suppressed by TEA, a blocker of BK(Ca), HS-142-1, a blocker of GC-coupled NPRs, or methylene blue (MB), a selective inhibitor of guanylyl cyclase. Sequentially, whole-cell K(+) currents were recorded using patch clamp techniques. BK(Ca) current of VSMCs isolated from rat mesentery artery was obtained by subtracting the whole cell currents after applications of 10(-7) mol/l iberiotoxin (IBX) from before its applications. In accordance with the results of arterial tension detection, BK(Ca) current was significantly magnified by VNP, which could also be mimicked by 8-Br-cGMP, whereas suppressed by HS-142-1, or MB. Taken together, VNP acts as a potent vasodilator, and NPRA/B-cGMP-BK(Ca) is one possible signaling system involved in VNP induced relaxation.