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

乙酰胆碱（Acetylcholine, ACh, 10 μM）刺激豚鼠胃窦黏液细胞引起细胞收缩，激活细胞内Ca^<2+>浓度（[Ca^<2+>]i）介导的胞吐事件，并通过细胞收缩调节乙酰胆碱诱发的胞吐。低氧胁迫的应用、无Cl^-溶液的输注和布美他尼的加入，导致[Cl^-]i的减少，增强了乙酰胆碱诱发的胞外事件。这些表明[Cl^-]i的减少似乎增强了乙酰胆碱诱发的胞外事件。用制霉菌素处理分离的胃窦黏液细胞，改变[Cl^-]i。当[Cl^-li]从5 mM增加到155.5 mM时，乙酰胆碱诱发的胞外事件频率下降约50%。因此，[Cl-]i的减少增强了乙酰胆碱诱发的胞外事件。用抑制G蛋白的百日咳毒素（PTX）治疗，消除了乙酰胆碱诱发的胞吐的[Cl^-]i依赖性。Ca^<2+>-调节的胞外分泌由G蛋白调节，G蛋白对ptx敏感，并被胞内Cl^-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^-.