Do isolated gastric mucosal surface cells from rabbits secrete HCO3-?

Only indirect observations suggest that gastric surface cells secrete HCOH3-, which, if the case, should result in an alteration of intracellular pH. This study attempts to determine if HCO3- transport is notable in intracellular pH regulation by isolated surface cells. Maintenance of cellular pH during perfusion with HCO3(-)-free Ringer's solution is unaffected by either the absence of Cl- or the presence of an inhibitor of HCO3- transport, 4,4'-diisothiocyanostilbene-2-2'-disulfonate (DIDS). This implies the absence of Cl-/HCO3- exchange and HCO3- transport related to Na+. Addition of HCO3-/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 HCO3-/CO2. Removal of HCO3-/CO2 results in alkalinization, which is unaffected by the absence of Cl-. Alkalinization following HCO3-/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 HCO3- 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+.