中文摘要：

目的：乙酰胆碱（ACh）不仅是神经递质，也是一种有效的血管舒张物质参与许多血管床的调节活动。本实验观察ACh引起耳蜗螺旋动脉平滑肌细胞超极化的离子机制以及NO在超极化反应中的可能作用。方法：在豚鼠离体耳蜗螺旋动脉标本上，运用细胞内微电极技术记录外源性的ACh引起的反应。结果：在保持灌流液中含有5mmol／L K^＋以及最小纵向张力的情况下，ACh（0．1—10μmol／L）引起低静息膜电位细胞明显的超极化反应，而引起高静息膜电位细胞明显的去极化反应。ACh引起的平滑肌细胞超极化反应是浓度依赖性的（ACh的浓度是1μmol／L和10／μmol／L时，分别引起超极化的幅度是22和30mV，n=7）。ACh引起的超极化反应能被阿托品（atropine，0．1～1μmol／L，n=6）或DAMP（50～100nmol／L，n=6，一种选择性的地受体的拮抗剂）所阻断，同时也可被BAPTA—AM（10μmol／L，n=7，一种可通过细胞膜的Ca^2＋螯合剂）或eharybdotoxin＋apamin（50-100nmol／L，n=4，两种Ca^2＋激活K^＋通道的阻断剂）所阻断，但是Nω-nitro-L-arginine methyl ester（L-NAME，300μmol／L，n=8，一种NO合成酶的完全抑制剂，n≥5）或glipizide（10μmol／L，ATP敏感性的K^＋通道阻断剂，n=4）或indomethacin（10μmol／L，环氧合酶的抑制剂，n=4）不能阻断ACh引起的超极化反应。结论：ACh通过激活内皮细胞的M3受体，开放钙依赖的钾通道．进而引起耳蜗螺旋动脉平滑肌细胞产生超极化反应，并且这一超极化反应与内皮细胞NO的产生和释放无关。

英文摘要：

Aim： Acetylcholine（ACh） is a and a potent vasodilator in many vascular beds. ACh hyperpolarizes the smooth muscle cells（SMCs） of arteries including the cochlear spiral modiolar artery（SMA） via an endothelium-dependent mechanism, but the biochemical and biophysical basis of the hyperpolarization and vasodilation remain unclear and controversial. Methods： Using intracellular recording techniques and an in vitro preparation of the SMA, the ionic mechanism of the hyperpolarization and a possible role of nitric oxide（NO） were investigated. Results： With 5 mmol/L K^＋ in the bathing solution and a minimum longitudinal tension, ACh（0.1 - 10 μmol/L） induced a robust hyperpo- larization in low RP cells but caused a depolarization in the high RP cells. The ACh hyperpolarization was fast in onset and offset and the amplitude was concentration-dependent（22 and 30 mV by 1 μmol/L and 10 μmol/L ACh, respectively, n = 7 ）. ACh also hyperpola-rized the cells that initially had a high resting potential（RP） but were pre-depolarized by Ba^2＋ （50 - 100 μmol/L）. The onset time courses of the hyper- polarization were often slower in these cases than those without the presence of Ba^2 ＋ . The ACh-induced hyperpolarization was blocked by atropine （0.1 -1 μmol/L, n = 6） or DAMP（50- 100 nmol/L, n = 6, a selective M3 antagonist） and also by BAPTA-AM（10 μmol/L, n = 7, a membrane-permeable Ca^2＋ -chelator）, or charybdotoxin pins apamin（50 - 100 nmol/L, n = 4, Ca^2＋ -activated K^＋ -channel blockers）, but not by Nω-nitro-L-arginine methyl ester（L-NAME, 300 μmol/L, n = 8, an inhibitor of NO-synthase）, glipizide（ 10 μmol/L, n = 4, ATP- sensitive K^＋ -channel blocker） and indomethacin（ 10 μmol/L, n = 4, cyclo-oxygenase inhibitor）. Conclusion： It is concluded that ACh-induced hyperpolarization in the arterial SMCs is primarily due to an activation of calcium-activated potassium channels via M3 receptors of endothelial cell and is independent of NO-release in