SMOOTH-MUSCLE HYPERPOLARIZATION AND RELAXATION TO ACETYLCHOLINE IN THE RABBIT BASILAR ARTERY

Acetylcholine-evoked relaxation of noradrenaline-stimulated segments o f the rabbit basilar artery was accompanied by a small, transient hype rpolarization of the smooth muscle cell membrane which was diminished by repeated exposure to the agonist. In the presence of glibenclamide (10 mu M) or high concentrations of potassium chloride (65 mM), the ac etylcholine-evoked smooth muscle hyperpolarization was abolished, wher eas the relaxation response was unaffected. Nitric oxide (NO gas in so lution; 0.5-15 mu M) evoked dose-dependent relaxation in noradrenaline contracted arterial segments, but had no effect on the smooth muscle membrane potential, even at a saturated concentration (150 mu M), whic h was 10 times higher than required to stimulate maximal relaxation. A dditionally, NO-evoked relaxations were unaffected by glibenclamide (1 0 mu M), but the responses were significantly attenuated in the presen ce of 65 mM potassium chloride. These data show that, as in the rabbit middle cerebral artery, acetylcholine-evoked hyperpolarization in the rabbit basilar artery is mediated by glibenclamide-sensitive potassiu m channels. However, in contrast to the middle cerebral artery and to other vessels such as the rat mesenteric artery, the change in smooth muscle membrane potential does not make an important contribution to t he relaxation evoked either by this agonist or by NO.