Nitric oxide induced membrane hyperpolarization in the rat aorta is not mediated by glibenclamide-sensitive potassium channels.

Using conventional intracellular microelectrode techniques, the membrane potential (Em) of vascular smooth muscle cells in isolated segments of thoracic rat aorta was measured. The influence of exogenous and of endothelium-derived nitric oxide on the Em was assessed, and the involvement of glibenclamide-sensitive channels in the observed membrane hyperpolarization was investigated. Exposures of the aorta strips to sodium nitroprusside (10(-8)-10(-5) M) caused a concentration-dependent and endothelium-independent hyperpolarization. Maximal hyperpolarization (5.7 +/- 0.4 mV) was obtained with 10(-5) M sodium nitroprusside. Acetylcholine (10(-8)-10(-5) M produced endothelium-dependent hyperpolarizations. At low concentrations, a slow Em change was elicited, which was sustained in the presence of the vasodilator. Higher concentrations of acetylcholine caused hyperpolarizations consisting of an initial transient peak followed by a more sustained component. Pre-exposure to Ng-nitro-L-arginine (L-NNA, 2 x 10(-4) M), which depolarized Em by 2.5 +/- 0.7 mV, significantly attenuated the later component of hyperpolarizations, indicating that it is NO dependent. Glibenclamide (10-5 M) did not significantly affect the hyperpolarization induced by 10(-6)-10(-5) M sodium nitroprusside nor the maintained component of hyperpolarization induced by 10(-5) M acetylcholine. It is concluded that the hyperpolarization caused by exogenous or endogenous NO in the rat aorta is not mediated by activation of glibenclamide-sensitive potassium channels.