Objective To determine the effects of 17 β-estradiol on cellular electrophysiology and L-type Ca2+ currents (L-ICa) induced by endothelin-1 (ET-1) in ventricular papillary muscles and myocytes of guinea pig.Methods Standard microelectrodes and whole cell patch clamp techniques were used to record the action potentials and L-ICa.Results Superfusion of ET-1 for 30 minutes resulted in a marked prolongation of the action potential duration (APD) without any significant changes of APA and Vmax in ventricular papillary muscles of guinea pigs. In additional 17 β-estradiol (30 μmol/L), APD was abbreviated. In the patch clamp study, ET-1 increased the mean peak L-ICa from 534.46±46.23 to 1003.15±39.12 (pA) with peak voltage-current curve shifting to left, and steady-state activation curve was shifted in depolarization direction in contrast to the steady-state inactivation curve. However, in additional 17 β-estradiol, the L-ICa decreased by 33.32% (P<0.01) with peak voltage-current curve shifting to right and, the deviation of the steady-state activation and inactivation curves caused by ET-1 was depressed.Conclusion 17 β-estradiol attenuates ET-1-induced prolongation of APD in guinea pig papillary muscles by an inhibitory effect on L-ICa in guinea pig ventricular myocytes, which may account for its antiarrythmic effect.