Effects of aspirin on pathways of ion permeation in Necturus antrum: role of nutrient HCO3.

Intracellular microelectrodes were used to evaluate electrical properties of the cell membranes in Necturus antral mucosa during exposure to luminal acid alone (pH 4) or to 5 mmol/L aspirin [acetylsalicylic acid (ASA)] in the presence of luminal acid. When nutrient solutions were buffered by HCO3- (pH 7.3), ASA moderately depolarized and increased the resistances of both cell membranes. When nutrient solutions were buffered by HEPES (pH 7.3), ASA induced even greater depolarizations of the cell membranes. In addition, resistance of the apical membrane did not increase and resistance of the basolateral membrane decreased. The changes in basolateral membrane resistance were observed when tissues were exposed to 5 mmol/L salicylate but not during exposure to luminal acid alone or to acidified luminal solutions containing 5 mmol/L acetate, a small and permeable organic acid. Electron microscopy confirmed that these initial electrophysiological changes precede alterations in cell morphology. The findings suggest that nutrient HCO3- attenuates changes in membrane potentials caused by ASA. Loss of nutrient HCO3- seems to accelerate alterations in basolateral membrane resistance caused by ASA and its salicylate moiety.