Histamine reduces Cl? activity in surface epithelial cells of frog gastric mucosa

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Abstract
Intracellular chloride activity (a c Cl ) and serosal as well as mucosal membrane potentials (Vcs andVcm) were recorded in surface epithelial cells (SEC) of frog gastric mucosa during the resting state (cimetidine, 10−4 mol/l) or during stimulation with histamine (10−4 mol/l). Stimulation leads to a fall ina c Cl from 18.7 SD±5.9 mmol/l (n=26) to 13.3 SD±4.9 mmol/l (n=33). Simultaneously both cell membranes hyperpolarize,Vcs from −56.0 SD±4.8 (n=42) to −62.8±7.6 (n=43) andVcm from −39.6 SD±5.8 (n=42) to −47.9±7.6 (n=43), so that intracellular chloride remains elevated above electrochemical equilibrium at both cell membranes. Reduction or omission of chloride in the lumen perfusate does not affecta c Cl , suggesting that the luminal cell membrane is virtually tight for chloride ions. Current induced hyperpolarization of the serosal cell membrane potential which simulates the electrical effects of stimulation, does not affecta c Cl either; however, inhibition of gastric acid secretion by a benzimidazol derivative which is known to block the H+/K+ ATPase prevents the fall ina c Cl in response to histamine. The same holds if the experimental solutions are gassed with 25% CO2 which does not interfere with acid secretion but may block cell to cell communication via gap junctions. From these results we conclude that 1. the SEC are not involved in non-acidic Cl− secretion, neither in resting nor in stimulated state, and 2. that the fall ina c Cl of the surface epithelial cells under stimulation does not seem to reflect a direct action of histamine on the SEC but seems to reflect a fall ina c Cl of the oxyntic cells which may be coupled to the surface epithelial cells by permeable cell-to-cell junctions.