Abstract

The effects of [Cl−]i on ACh‐stimulated exocytosis were studied in guinea pig antral mucous cells. ACh activated Ca2+‐regulated exocytosis (initial phase followed by a sustained phase). Bumetanide or an NO3− solution enhanced it, in contract, NPPB decreased it and eliminated the enhancement. ATP depletion studies demonstrated that exposure of NO3− solution prior to ATP depletion induced an enhanced initial phase followed by a sustained phase, whereas exposure of NO3− solution after ATP depletion induced only a sustained phase. Measurements of [Cl−]i revealed that ACh decreases [Cl−]i. and that bumetanide and NO3− solution decreased [Cl−]i and enhanced the ACh‐evoked [Cl−]i decrease; in contrast, NPPB increased [Cl−]i and inhibited the [Cl−]i decrease induced by ACh, bumetanide or NO3− solution. [Ca2+]i measurements showed that a decrease in [Cl−]i enhanced the ACh‐stimulated [Ca2+]i increase. In conclusion, a decrease in [Cl−]i accelerates ATP‐dependent priming and [Ca2+]i increase, which enhance Ca2+‐regulated exocytosis in ACh‐stimulated antral mucous cells.

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