Plane F, Garland C J
Department of Physiology and Pharmacology, University of Southampton, UK.
J Auton Nerv Syst. 1994 Sep;49 Suppl:S15-8. doi: 10.1016/0165-1838(94)90080-9.
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.
乙酰胆碱引起的兔基底动脉去甲肾上腺素刺激节段的舒张，伴随着平滑肌细胞膜的小幅短暂超极化，反复暴露于激动剂后该超极化减弱。在格列本脲（10微摩尔）或高浓度氯化钾（65毫摩尔）存在的情况下，乙酰胆碱引起的平滑肌超极化被消除，而舒张反应不受影响。一氧化氮（溶液中的一氧化氮气体；0.5 - 15微摩尔）在去甲肾上腺素收缩的动脉节段中引起剂量依赖性舒张，但即使在饱和浓度（150微摩尔，比刺激最大舒张所需浓度高10倍）下，对平滑肌膜电位也没有影响。此外，一氧化氮引起的舒张不受格列本脲（10微摩尔）影响，但在65毫摩尔氯化钾存在时反应显著减弱。这些数据表明，与兔大脑中动脉一样，兔基底动脉中乙酰胆碱引起的超极化由格列本脲敏感的钾通道介导。然而，与大脑中动脉和其他血管如大鼠肠系膜动脉不同，平滑肌膜电位的变化对该激动剂或一氧化氮引起的舒张没有重要贡献。
