Intracellular chloride activity (acCl) and serosal as well as mucosal membrane potentials (Vcs and Vcm) 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 in acCl 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) and Vcm 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 affect acCl, 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 affect acCl either; however, inhibition of gastric acid secretion by a benzimidazol derivative which is known to block the H+/K+ ATPase prevents the fall in acCl 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.(ABSTRACT TRUNCATED AT 250 WORDS)