Exocytosis regulation of [Cl^-]i and G protein in gastric mucous cells.

乙酰胆碱（ACh，10 μM）刺激豚鼠胃窦粘液细胞，引起细胞收缩和胞内Ca^2+浓度（[Ca^2+]i）介导的胞吐事件的激活，ACh诱发的胞吐受细胞收缩的调节。应用低渗应激、输注不含Cl^-的溶液和加入布美他尼（可导致[Cl^-]i减少）可增强ACh诱发的胞吐事件。这些结果表明，[Cl^-]i的降低似乎增强了乙酰胆碱诱发的胞吐事件。用制霉菌素处理离体胃窦粘液细胞以改变[Cl^-]i。当[Cl^-] i从5 mM增加到155.5 mM时，乙酰胆碱诱发的胞吐事件的频率下降约50%。因此，[Cl-]i的减少增强了ACh诱发的胞吐事件。百日咳毒素（PTX）可以抑制G蛋白，因此可以消除乙酰胆碱诱发的胞吐作用对[Cl^-]i的依赖性。Ca^2+调节的胞吐作用受到G蛋白的调节，G蛋白对PTX敏感，并受细胞内Cl^-的抑制。

Acetylcholine (ACh, 10 μM) stimulation caused cell shrinkage and activation of exocytotic events mediated via intracellular Ca^<2+> concentration ([Ca^<2+>]i) in antral mucus cells of guinea pig, and ACh- evoked exocytosis was modulated by cell shrinkage. Application of a hyposmotic stress, infusion of Cl^--free solution and addition of bumetanide, which caused reduction of [Cl^-]i, potentiated ACh- evoked exocytotic events. These indicate that decreases in [Cl^-]i appears to potentiate ACh-evoked exocytotic events. Isolated antral mucus cells were treated with nystatin to alter [Cl^-]i. As [Cl^-li increase from 5 to 155.5 mM, the frequency of ACh-evoked exocytotic events declines approximately 50%. Thus, reduction of [Cl-]i potentiated ACh-evoked exocytotic events. Treatment with pertussis toxin (PTX), which inhibits G proteins, eliminated the [Cl^-]i dependency of ACh-evoked exocytosis. The Ca^<2+>-regulated exocytosis was modulated by G proteins, which are PTX-sensitive and inhibited by intracellular Cl^-.