Experiments were designed to determine the subtype of potassium channels activated by the nitrovasodilator 3-morpholinosydnonimine (SIN-1). Membrane potential was recorded by means of intracellular microelectrodes inserted from the adventitial side, in the vascular smooth muscle cells of isolated segments of the carotid artery of the guinea-pig, superfused with thermostated. modified Krebs-Finger bicarbonate solution (containing N-omega-nitro-L-arginine and indomethacin). Potassium currents were recorded, at room temperature, in freshly dissociated smooth muscle cells from both preparations by the patch clamp technique (whole-cell, cell-attached, and excised configurations). SIN-1 caused a significant hyperpolarization of the smooth muscle cells of the guinea-pig carotid artery. The effects of SIN-1 were not affected by apamin, charybdotoxin, or the combination of the two toxins, but were abolished by glibenclamide. In freshly dissociated smooth muscle cells of the guinea-pig carotid artery, SIN-1 induced small or no modification of the whole-cell potassium current and of the iberiotoxin-sensitive potassium current, measured with the patch clamp technique (cell-attached configuration). However, the nitrovasodilator activated a small glibenclamide-sensitive current. In contrast, in freshly dissociated smooth muscle cells of the rabbit aorta, SIN-1 enhanced the activity of the global potassium current and of the iberiotoxin-sensitive potassium current. These findings suggest that the effects of NO in vascular smooth muscle are species-dependent. It activates ATP-sensitive potassium channels in smooth muscle cells of the guinea pig carotid artery and large conductance calcium-sensitive potassium channels in smooth muscle cells of the rabbit aorta. This results further confirm that NO and EDHF (which activates a glibenclamide-insensitive potassium conductance) are different in the guinea-pig carotid artery.