Effects of cyclic adenosine monophosphate and prostaglandins on Na+- and HCO3−-induced dissipation of a proton gradient in isolated gastric mucosal surface cells of rabbits

Abstract

One mechanism that surface cells can use to regulate intracellular pH is Na+/H+ exchange. The presence of another means to modify intracellular pH, HCO3−, was investigated, as were the effects of cyclic adenosine monophosphate and prostaglandins on an intracellular proton gradient. Isolated surface cells were preincubated in NH4+ to establish an intracellular proton gradient, which was measured using acridine orange. The addition of HCO3− causes gradient dissipation, an effect sensitive to 4-acetamido-4′-isothiocyanostilbene-2,2′-disulfonic acid but not to extracellular chloride. The HCO3−-evoked dissipation of the proton gradient is diminished by cyclic adenosine monophosphate, isobutylmethylxanthine, and prostaglandin E2, but not by prostacyclin. The Na+-evoked dissipation of the gradient is diminished by cyclic adenosine monophosphate and isobutylmethylxanthine, but not by prostaglandin E2 or prostacyclin. Cyclic adenosine monophosphate, isobutylmethylxanthine, and the prostaglandins are without effect in the absence of Na+ or HCO3−. The data suggest that extracellular HCO3− influences an intracellular proton gradient, but the precise mechanism involved is not established in this study. The data may also explain why prostaglandins are in some instances not cytoprotective for surface cells.