Acid pH and weak acids induce Na−Cl contransport in the rabbit urinary bladder

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Abstract
We have described a coupled Na−Cl entry step at the apical membrane of a tight epithelium, the rabbit urinary bladder. Mucosal pH values, more acid than 4.6, stimulate a 20 to 40-fold increase in mucosal-to-serosal Na+ and Cl− flux. The flux increase is almost completely blocked by low concentrations of bumetanide. The transepithelial movement of Na+ and Cl− is normally electroneutral; however, when weak acids (such as acetate) are present in the mucosal solution, the acid-induced increase in flux is accompanied by a large increase in short-circuit current. Besides blockage by bumetanide, both the increase in flux and short-circuit current are blocked by: (1) Na+-free solutions on the mucosa; (2) Cl−-free solutions on the mucosa; (3) phosphodiesterase inhibitors; (4) ouabain in the serosal solution; (5) K+-free solutions on the serosa; and (6) HCO 3 − -free solutions on the serosa. The increase in the fluxes and the short-circuit current is unaffected by: (1) amiloride application in the mucosal solution; (2) mucosally applied stilbene derivatives which block Cl−/HCO 3 − exchange (SITS); and (3) Cl−-free solutions applied to the serosa. We interpret these results to imply a coupled Na−Cl uptake step at the apical membrane which is stimulated by intracellular acetate (or pH). The uptake step leads to a movement of Na+ and Cl− across the basolateral membrane, which is mediated by the Na+, K+-ATPase and a Na/Cl/HCO 3 − exchange mechanism. Our results demonstrate that “tight” epithelia may, under appropriate circumstances, demonstrate mechanisms of ion movement which are similar to “leaky” epithelia.