Lu T, Huang Y, Jiang W
Laboratory of Cardiology, First Affiliated Hospital of Suzhou Medical College.
Chin Med J (Engl). 1995 Aug;108(8):618-25.
To study the electrophysiologic effects of endothelin-1 (ET-1), we used patch clamp and glass microelectrode techniques to investigate the effects of ET-1 on cardiac L-Ica, Ik and Ik2 in guinea pig ventricular myocytes. The prolongation of APD50 was induced and EADs was triggered by 50 nM ET-1 perfusion. L-Ica and Ik were enhanced by various ET-1 concentration from 1 to 50 nM with dose-dependence. Their steady-state activations of L-Ica and Ik shifted left with ET-1 concentration increments. ET-1 elicited a kind of GTP-dependent inward rectifier K+ current having a mean conductance of 82.36 +/- 1.27 pS. The open time and close time (both interburst intervals and burst durations) abbreviated with ET-1 concentration increase. The results suggested that EADs -ET evoked was ascribed to the prolongation on the plateau level, which resulted from L-Ica enhancement. The ET- evoked inward rectifier K+ current should be further studied.
为研究内皮素-1(ET-1)的电生理效应,我们采用膜片钳和玻璃微电极技术,研究ET-1对豚鼠心室肌细胞心脏L型钙电流(L-Ica)、钾电流(Ik)和内向整流钾电流(Ik2)的影响。50 nM ET-1灌注可诱导动作电位时程50%(APD50)延长并触发早期后除极(EADs)。1至50 nM不同浓度的ET-1可增强L-Ica和Ik,且具有剂量依赖性。随着ET-1浓度增加,L-Ica和Ik的稳态激活向左移位。ET-1引发一种平均电导为82.36±1.27 pS的GTP依赖性内向整流钾电流。开放时间和关闭时间(包括爆发间期和爆发持续时间)均随ET-1浓度增加而缩短。结果表明,ET-1诱发的EADs归因于L-Ica增强导致的平台期延长。ET-1诱发的内向整流钾电流有待进一步研究。