REGULATION OF INTRACELLULAR PH IN ISOLATED NECTURUS GASTRIC-MUCOSA DURING SHORT-TERM EXPOSURE TO LUMINAL ACID

Background/Aims: Continuous exposure to gastric acid implies efficient control mechanisms of intracellular pH (pH(i)) in the gastric epithel ium. This study assessed the roles of Na+, H+, and HCO3- transport mec hanisms in controlling pH(i) during short-term exposure of the gastric epithelium to luminal acid. Methods: pH(i) and Na+ activity (a(Na)(i) ) were measured with liquid sensor microelectrodes in isolated Necturu s antral mucosa, modulating ion transport mechanisms by ion removal an d pharmacological inhibition. Results: Shortterm exposure to luminal a cid (pH 2.3) acidified pH(i) by 0.3 pH units, whereafter pH(i) stabili zed. This was associated with transient increase in a(Na)(i). Blocking of Na+/H+ exchange (in the presence of HCO3-/CO2) by removal of Na+ o r addition of amiloride eliminated the increase in a(Na)(i) and result ed in uncontrolled acidification of pH(i). Similarly, blocking of HCO3 - transport (in the presence of Na+) by removal of HCO3-/CO2 or additi on of -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). Concl usions: The data indicate that during short-term exposure of the gastr ic mucosa to luminal acid, both Na+/H+ antiport and HCO3- transport ar e needed to control pH(i) and maintain it within physiological ranges.