Mechanism of luminal alkalinization by bullfrog fundic mucosa.

Metiamide-inhibited fundic mucosa of bullfrog secreted alkali (OH-) at 0.1-0.2 mueq.cm-2.h-1.OH- was abolished by dinitrophenol (DNP) and was decreased significantly by 4,4-didsothiocyano-2,2-disulfonate stilbene (DIDS), anoxia, or HCO3(-)-free nutrient solution. In Na+ solutions, increasing nutrient, [HCO3(-)] augmented OH- and Isc linearly while resistance (R) decreased. No such changes occurred in Na+-free nutrient solution. In all experiments, delta Isc was approximately 12 X delta OH. Replacement of Cl- in the secretory solutions or in the nutrient solutions had no significant influence on OH-. When Na+-free nutrient solutions and Cl--free secretory solutions were present, OH- decreased significantly (P less than 0.01). Increasing nutrient [Cl-] in the absence of secretory Cl- significantly (P less than 0.01) augmented OH- and Isc. In the absence of secretory Cl-, OH- and Isc were linearly related to varying nutrient [Cl-]. In tissues with nutrient solutions on the secretory side and vice versa, apparent OH- was 0.4-0.5 mueq.cm-1.h-1 and was dependent on secretory [HCO3(-)] but was not affected by DNP, DIDS, or replacement of Cl- on secretory or nutrient solutions. We conclude that 1) OH- secretion is dependent on nutrient HCO3(-) and Na+ and oxidative metabolism, 2) endogenous HCO3(-) does not contribute significantly, and 3) adequate tissue Cl- must be present for normal OH-.