Mechanism of luminal alkalinization by bullfrog fundic mucosa

Metiamide-inhibited fundic mucosa of bullfrog secreted alkali (OH^-) at 0.1-0.2 μeq.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 I(sc) linearly while resistance (R) decreased. No such changes occurred in Na⁺-free nutrient solution. In all experiments, ΔI(sc) was ~12 x ΔOH. 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 < 0.01). Increasing nutrient [Cl^-] in the absence of secretory Cl^- significantly (P < 0.01) augmented OH^- and I(sc). In the absence of secretory Cl^-. OH^- and I(sc) 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 μeq.cm^-2.h^-1 and was dependent on secretory [HCO₃ ^-] but was 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^-.