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To study the electrophysiologlc effects of endothelin-1 (ET-I), we used patch clamp and glass microelectrode techniques to investigate the effects of ET-1 on cardiac L-Ica, Ik and lk_2 in guinea pig ventricular myocytes. The prolongation of APD_50 was induced and EADs was triggered by 50 nM ET-I perfusion. L-Ica and Ik were enhanced by various ET-I concentration from I 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 inhancement. The ET- evoked inward rectifier K~+ current should be further studied.
To study the electrophysiologlc effects of endothelin-1 (ET-I), we used patch clamp and glass microelectrode techniques to investigate the effects of ET-1 on cardiac L-Ica, Ik and lk_2 in guinea pig ventricular myocytes. The prolongation of APD_50 L-Ica and Ik were enhanced by various concentrations of ET-I from 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 inhancement. The ET-evoked inward rectifier K ~ + current should be further studied.