HCO₃-secretion by bullfrog duodenum: Dependence on nutrient Na⁺ during secretory stimulation

HCO₃^- secretion across in vitro duodenal mucosa of Rana catesbeiana was investigated under baseline conditions and during secretory stimulation. Baseline secretion was abolished by removal of CO₂-HCO₃- and reduced ~60% by removal of nutrient Na⁺, but was not sensitive to changes in Cl^- or K⁺. Baseline secretion was not directly altered by exposure to 10^-3 M amiloride or 10^-3 M H₂DIDS (dihydro-4,4'-diisothiocyanostilbene-2,2'-disulfonic acid) in the nutrient solution and only mildly reduced by acetazolamide. Following removal and restoration of Na⁺, recovery of secretion was impaired by exposure to acetazolamide (5 x 10^-4 M) or H₂DIDS (5 x 10^-4 M) in the nutrient solution. Secretion stimulated by glucagon (10^-6 M) or 16,16- dimethyl prostaglandin E₂ (10 μg · mL^-1) was markedly attenuated by removal of Na⁺ or by exposure to H₂DIDS, but secretion was not altered by acetazolamide (5 x 10^-4 M) or nutrient amiloride (1 mM). Thus, the HCO₃^- that is secreted under nonstimulated conditions derives partly from basolateral Na⁺-dependent uptake and partly from cellular CO₂ hydration. Secretagogue-stimulated secretion by duodenal surface epithelium depends on stilbene-sensitive Na⁺(HCO₃^-), uptake across the basolateral membrane.