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

HCO3- secretion across in vitro duodenal mucosa of Rana catesbeiana was inv estigated under baseline conditions and during secretory stimulation. Basel ine secretion was abolished by removal of CO2-HCO3- and reduced similar to 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 ami loride or 10(-3) M H2DIDS (dihydro-4,4'-diisothiocyanostilbene-2,2'-disulfo nic acid) in the nutrient solution and only mildly reduced by acetazolamide . Following removal and restoration of Na+, recovery of secretion was impai red 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(-4) M) or 16,1 6-dimethyl prostaglandin E-2 (10 mu g mL(-1)) was markedly attenuated by re moval of Na+ or by exposure to H2DIDS but secretion was not altered by acet azolamide (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-sen sitive Na+(HCO3-)(n) uptake across the basolateral membrane.