4-Aminopyridine-sensitive K+ channels contributes to NaHS-induced membrane hyperpolarization and relaxation in the rat coronary artery
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摘要The present study aimed at examining the role of potassium channels and endothelium in relaxations induced by sodium hydrogen sulphide (NaHS), which is the donor of gaseous hydrogen sulphide (H2S) and the effect of NaHS on endothelium-dependent relaxations in rat coronary arteries. Rat coronary arteries were suspended in a myograph for force measurement and changes of the membrane potential in arteries were determined by membrane potential-sensitive fluorescence dye. NaHS relaxed coronary arteries pre-contracted by U46619 and the relaxation was significantly less in high KCl-contracted rings. NaHS-induced relaxations were reduced by 4-aminopyridine (4-AP) but unaffected by glibenclamide, iberiotoxin, N-G-nitro-L-arginine methyl ester, ODQ indomethacin or by endothelium removal. The inhibitory effect of 4-AP was absent in NaHS-induced relaxations in high KCl-contracted rings. Addition of NaHS caused membrane hyperpolarization and this effect was inhibited by 4-AP but not by glibenclamide. NaHS causes endothelium-independent relaxations in rat coronary arteries partially through activation of 4-AP-sensitive potassium channel and ensuring hyperpolarization. Other potassium channels. Na+-K+ pump or endothelium-derived relaxing factors play little role. (C) 2010 Elsevier Inc. All rights reserved.
著者Cheang WS, Wong WT, Shen B, Lau CW, Tian XY, Tsang SY, Yao XQ, Chen ZY, Huang Y
期刊名稱Vascular Pharmacology
出版年份2010
月份9
日期1
卷號53
期次3-4
出版社ELSEVIER SCIENCE INC
頁次94 - 98
國際標準期刊號1537-1891
電子國際標準期刊號1879-3649
語言英式英語
關鍵詞Coronary artery; Hydrogen sulphide; Potassium channel; Rat; Relaxation
Web of Science 學科類別Pharmacology & Pharmacy; PHARMACOLOGY & PHARMACY

上次更新時間 2020-17-11 於 00:23