Smooth muscle hyperpolarization and relaxation to acetylcholine in the rabbit basilar artery

Acetylcholine-evoked relaxation of noradrenaline-stimulated segments of the rabbit basilar artery was accompanied by a small, transient hyperpolarization of the smooth muscle cell membrane which was diminished by repeated exposure to the agonist. In the presence of glibenclamide (10 microM) or high concentrations of potassium chloride (65 mM), the acetylcholine-evoked smooth muscle hyperpolarization was abolished, whereas the relaxation response was unaffected. Nitric oxide (NO gas in solution; 0.5-15 microM) 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 microM), which was 10 times higher than required to stimulate maximal relaxation. Additionally, NO-evoked relaxations were unaffected by glibenclamide (10 microM), but the responses were significantly attenuated in the presence 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 potassium 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 the relaxation evoked either by this agonist or by NO.