摘要
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-lea and Ik were enhanced by various ET-1 concentration from 1 to 50 nM with dose-dependence. Their steady-state activations of L-Iea 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 inhancement. The ET- evoked inward rectifier K+ current should be further studied.
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-lea and Ik were enhanced by various ET-1 concentration from 1 to 50 nM with dose-dependence. Their steady-state activations of L-Iea 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 inhancement. The ET- evoked inward rectifier K+ current should be further studied.
