3-Morpholinosydnonimine (SIN-1) and K + channels in smooth muscle cells of the rabbit and guinea pig carotid arteries

Experiments were designed to determine the subtype of K + channels activated by the nitrovasodilator 3-morpholinosydnonimine (SIN-1) in smooth muscle cells of the rabbit and guinea pig carotid arteries. Membrane potential was recorded in isolated segments with intracellular microelectrode and K + currents in freshly dissociated smooth muscle cells, with the patch–clamp technique. In the guinea pig carotid artery, SIN-1 caused a glibenclamide-sensitive hyperpolarization. The nitrovasodilator did not affect the whole-cell K + current, but activated a glibenclamide-sensitive K + current. In the rabbit carotid artery, SIN-1 induced only an iberiotoxin-sensitive repolarization in phenylephrine-depolarized tissue and in isolated cells, enhanced the activity of an iberiotoxin-sensitive K + current. These findings demonstrate that the population of K + channels activated by nitric oxide (NO) is species-dependent and support the conclusion that, in the guinea pig carotid artery, in contrast to the rabbit carotid artery, the release of NO cannot account for the responses attributed to endothelium-derived hyperpolarizing factor (EDHF).