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.
|Original language||English (US)|
|Number of pages||8|
|Journal||Chinese medical journal|
|State||Published - Aug 1995|
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