4-aminopyridine-sensitive K+ channels contributes to NaHS-induced membrane hyperpolarization and relaxation in the rat coronary artery.
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 (H(2)S) 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.
Cheang
Wai San
WS
Li Ka Shing Institute of Health Sciences, Chinese University of Hong Kong, Hong Kong, China.
Wong
Wing Tak
WT
Shen
Bing
B
Lau
Chi Wai
CW
Tian
Xiao Yu
XY
Tsang
Suk Ying
SY
Yao
Xiaoqiang
X
Chen
Zhen Yu
ZY
Huang
Yu
Y
D015761:4-Aminopyridine / Q000494:pharmacology*; D000818:Animals; D001685:Biological Factors / Q000378:metabolism; D003331:Coronary Vessels / Q000187:drug effects* / Q000502:physiology; D004730:Endothelium, Vascular / Q000502:physiology; D066298:In Vitro Techniques; D008297:Male; D008564:Membrane Potentials / Q000187:drug effects; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects* / Q000502:physiology; D026902:Potassium Channel Blockers / Q000494:pharmacology*; D015221:Potassium Channels / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013440:Sulfides / Q000494:pharmacology*; D014664:Vasodilation / Q000187:drug effects; D014665:Vasodilator Agents / Q000494:pharmacology*
D001685:Biological Factors; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D013440:Sulfides; D014665:Vasodilator Agents; C067410:endothelium-dependent hyperpolarization factor; D015761:4-Aminopyridine; C025451:sodium bisulfide