美西律通过激活ATP敏感性钾通道诱导心室肌动作电位时程缩短。
Mexiletine-induced shortening of the action potential duration of ventricular muscles by activation of ATP-sensitive K+ channels.
作者信息
Sato T, Shigematsu S, Arita M
机构信息
Department of Physiology, Oita Medical University School of Medicine, Japan.
出版信息
Br J Pharmacol. 1995 Jun;115(3):381-2. doi: 10.1111/j.1476-5381.1995.tb16342.x.
Abstract
A class Ib antiarrhythmic drug, mexiletine (100 microM) significantly shortened the action potential duration (APD) of guinea-pig ventricular muscles and this effect was completely abolished in the presence of glibenclamide (50 microM), a blocker of the ATP-sensitive K+ channel (KATP). Mexiletine significantly increased the open probability of uridine diphosphate-primed KATP channels, recorded in inside-out patches of the ventricular cells. The results suggest that mexiletine shortens the APD of ventricular muscles, at least in part, via activation of KATP.
摘要
I类抗心律失常药物美西律（100微摩尔）可显著缩短豚鼠心室肌动作电位时程（APD），而在存在格列本脲（50微摩尔）时，这种作用完全消失，格列本脲是一种ATP敏感性钾通道（KATP）阻滞剂。美西律可显著增加在心室细胞内向外膜片上记录的尿苷二磷酸引发的KATP通道的开放概率。结果表明，美西律至少部分通过激活KATP来缩短心室肌的APD。
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