Luminal H+ secretion by gastric mucosa is accompanied by basolateral HCO3- release. A basolateral Cl-/HCO3- exchanger is known to mediate HCO3- extrusion from oxyntopeptic cells during resting and secretagogue-induced apical HCl secretion. From recent work, we hypothesized that there might be a Cl--independent pathway for basolateral HCO3- exit in Necturus oxyntopeptic cells. In this study, we used a fluorescent pH indicator [2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein] to evaluate Cl--independent HCO3- transport across the basolateral membranes of intact oxyntopeptic cells. Removal of serosal Cl- increased intracellular pH (pHi) (7.05 to 7.25), consistent with Cl--dependent HCO3- extrusion. Removal of serosal Na+ in the absence of Cl- resulted in significant acidification of pHi (7.10 to 6.89), but studies involving amiloride, 4,4′-diisothiocyanostilbene-2,2′-disulfonic acid (BIDS), and 0 HCO3--N-2-hydroxyethylpiperazine-N′-2-ethanesulfonic acid-buffered solutions suggest that Na+-dependent changes in pHi are due to Na+/H+ exchange. Our studies demonstrate a marked concentration-dependent alkalinization when tissues are exposed to increases in serosal K+. A substantial part of this alkalinization in response to increases in serosal K+ (pHi 7.00 to 7.46) appears to be a HCO3- exit pathway that is independent of both Na+ and Cl-, unaffected by bumetanide or amiloride, but sensitive to DIDS. We propose the presence of a Cl-- and Na+-independent K+-dependent HCO3- cotransporter in Necturus oxyntopeptic cell basolateral membranes.
All Science Journal Classification (ASJC) codes
- Physiology (medical)