Do Isolated Gastric Mucosal Surface Cells from Rabbits Secrete HCO-3?

Abstract

Only indirect observations suggest that gastric surface cells secrete HCOH-3, which, if the case, should result in an alteration of intracellular pH. This study attempts to determine if HCO-3 transport is notable in intracellular pH regulation by isolated surface cells. Maintenance of cellular pH during perfusion with HCO-3-free Ringer's solution is unaffected by either the absence of Cl- or the presence of an inhibitor of HCO-3 transport, 4,4′-diisotbiocyanostilbene-2-2′-disulfonate (DIDS). This implies the absence of Cl-/HCO-3 exchange and HCO-3 transport related to Na+. Addition of HCO-3/CO2 to the perfusate results in acidification due to CO2. The pH then drifts upward, which is prevented by amiloride, an inhibitor of Na+/H+ exchange. Calculated H+ efflux is not significantly affected by HCO-3/CO2. Removal of HCO-3/CO2 results in alkalinization, which is unaffected by the absence of Cl. Alkalinization following HCO-3/CO2 removal is significantly impaired by acetazolamide. Once alkalinization occurs, the pH declines slowly and is unaffected by a Cl-free perfusate or amiloride or conductance but is markedly accelerated by a Na+-free perfusate. The latter is prevented by amiloride but not by DIDS. Thus, under isolated conditions, gastric mucosal surface cells do not appear to be a major source of HCO-3 secretion. Alkalinization of the cells can occur as a result of carbonic anhydrase activity, but the alkalinization is maintained by an extracellular Na+ gradient that prevents exchange of intracellular Na+ with extracellular H+.