BACKGROUND/AIMS: Continuous exposure to gastric acid implies efficient control mechanisms of intracellular pH (pHi) in the gastric epithelium. This study assessed the roles of Na+, H+, and HCO3- transport mechanisms in controlling pHi during short-term exposure of the gastric epithelium to luminal acid. METHODS: pHi and Na+ activity (aiNa) were measured with liquid sensor microelectrodes in isolated Necturus antral mucosa, modulating ion transport mechanisms by ion removal and pharmacological inhibition. RESULTS: Short-term exposure to luminal acid (pH 2.3) acidified pHi by 0.3 pH units, whereafter pHi stabilized. This was associated with transient increase in aiNa. Blocking of Na+/H+ exchange (in the presence of HCO3-/CO2) by removal of Na+ or addition of amiloride eliminated the increase in aiNa and resulted in uncontrolled acidification of pHi. Similarly, blocking of HCO3- transport (in the presence of Na+) by removal of HCO3-/CO2 or addition of 4-acetamido-4-isothiocyanatostilbene-2,2-disulfonic acid resulted in uncontrolled acidification of pHi despite increase in aiNa. Blocking of Na+/K+ exchange with ouabain eliminated the recovery of aiNa and also resulted in uncontrolled acidification of pHi. CONCLUSIONS: The data indicate that during short-term exposure of the gastric mucosa to luminal acid, both Na+/H+ antiport and HCO3- transport are needed to control pHi and maintain it within physiological ranges.
BACKGROUND/AIMS: Continuous exposure to gastric acid implies efficient control mechanisms of intracellular pH (pHi) in the gastric epithelium. This study assessed the roles of Na+, H+, and HCO3- transport mechanisms in controlling pHi during short-term exposure of the gastric epithelium to luminal acid. METHODS:pHi and Na+ activity (aiNa) were measured with liquid sensor microelectrodes in isolated Necturus antral mucosa, modulating ion transport mechanisms by ion removal and pharmacological inhibition. RESULTS: Short-term exposure to luminal acid (pH 2.3) acidified pHi by 0.3 pH units, whereafter pHi stabilized. This was associated with transient increase in aiNa. Blocking of Na+/H+ exchange (in the presence of HCO3-/CO2) by removal of Na+ or addition of amiloride eliminated the increase in aiNa and resulted in uncontrolled acidification of pHi. Similarly, blocking of HCO3- transport (in the presence of Na+) by removal of HCO3-/CO2 or addition of 4-acetamido-4-isothiocyanatostilbene-2,2-disulfonic acid resulted in uncontrolled acidification of pHi despite increase in aiNa. Blocking of Na+/K+ exchange with ouabain eliminated the recovery of aiNa and also resulted in uncontrolled acidification of pHi. CONCLUSIONS: The data indicate that during short-term exposure of the gastric mucosa to luminal acid, both Na+/H+ antiport and HCO3- transport are needed to control pHi and maintain it within physiological ranges.