Regulation of intracellular pH in isolated Necturus gastric mucosa during short-term exposure to luminal acid

Abstract

Background/Aims: Continuous exposure to gastric acid implies efficient control mechanisms of intracellular pH (pH i) in the gastric epithelium. This study assessed the roles of Na +, H +, and HCO 3 − transport mechanisms in controlling pH i during short-term exposure of the gastric epithelium to luminal acid. Methods: pH i and Na + activity (a i Na) were measured with liquid sensor microelectrodes in isolated Necturus antral mucosa, modulating ion transport mechanisms by ion removal and pharmacological inhibition. Results: Shortterm exposure to luminal acid (pH 2.3) acidified pH i by 0.3 pH units, whereafter pH i stabilized. This was associated with transient increase in a i Na. Blocking of Na +/H + exchange (in the presence of HCO 3 −/CO 2) by removal of Na + or addition of amiloride eliminated the increase in a Na i and resulted in uncontrolled acidification of pH i. Similarly, blocking of HCO 3 − transport (in the presence of Na +) by removal of HCO 3 − /CO 2 or addition of 4-acetamido-4-isothiocyanatostilbene-2,2-disulfonic acid resulted in uncontrolled acidification of pH i despite increase in a Na i. Blocking of Na +/K + exchange with ouabain eliminated the recovery of a Na i and also resulted in uncontrolled acidification of pH i. Conclusions: The data indicate that during short-term exposure of the gastric mucosa to luminal acid, both Na +/H + antiport and HCO 3 − transport are needed to control pH i and maintain it within physiological ranges.