4-Aminopyridine-sensitive K+ channels contributes to NaHS-induced membrane hyperpolarization and relaxation in the rat coronary artery
4-Aminopyridine-sensitive K+ channels contributes to NaHS-induced membrane hyperpolarization and relaxation in the rat coronary artery
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DOI：
10.1016/j.vph.2010.04.004
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发表时间：
2010-09-01
影响因子：
4
通讯作者：
Huang, Yu
中科院分区：
文献类型：
--
作者：
Cheang, Wai San;Wong, Wing Tak;Huang, Yu
本研究旨在探讨作为气态硫化氢（H2S）供体的硫化氢钠（NaHS）在大鼠冠状动脉舒张中的钾通道和内皮的作用，以及NaHS对冠状动脉内皮依赖性舒张的影响。将大鼠冠状动脉悬挂在肌图上测力，用膜电位敏感荧光染料测定动脉膜电位的变化。U46619使冠状动脉预收缩的NaHS松弛，高kcl收缩环的松弛程度明显降低。4-氨基吡啶（4-AP）可降低nahs诱导的松弛，但格列本脲、iberiotoxin、n - g -硝基- l -精氨酸甲酯、ODQ吲哚美辛或内皮去除对其无影响。4-AP对nahs诱导的高kcl收缩环松弛无抑制作用。NaHS的加入引起了膜的超极化，这种作用被4-AP抑制，而格列本脲没有抑制作用。NaHS部分通过激活4- ap敏感钾通道并确保超极化引起大鼠冠状动脉内皮非依赖性舒张。其他钾离子通道。Na+-K+泵或内皮源性舒张因子作用不大。(C) 2010爱思唯尔公司版权所有。
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.