We investigated the effects of endothelins on the membrane potential of vascular smooth-muscle cells of canine coronary artery, using glass microelectrodes. In tissues with endothelium, endothelin-1 (ET-1), from 10(-12) to 10(-9) M, did not alter the membrane potential. Higher concentrations of the peptide produced sustained depolarization without detectable hyperpolarization. Endothelin-3 (ET-3, 10(-11) to 10(-8) M) did not produce significant membrane hyperpolarization in tissues with endothelium. Prostaglandin F2 alpha (10(-5) M) depolarized the cell membrane by about 6 mV. ET-1 (10(-9) M) did not evoke detectable hyperpolarization in the presence of prostaglandin F2 alpha. In tissues incubated with BQ123 (10(-6) M, a selective ETA-receptor antagonist), which attenuated the depolarization evoked by ET-1, both isopeptides did not produce detectable hyperpolarization. These findings suggest that ET-1 and ET-3 do not evoke the release of endothelium-derived hyperpolarizing factor in the canine coronary artery.