Abstract
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-4,4prime-diisothiocyanostilbene-2,2prime-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 × 10-4 M) or H2DIDS (5 × 10-4 M) in the nutrient solution. Secretion stimulated by glucagon (10-6 M) or 16,16-dimethyl prostaglandin E2 (10 mu g·mL-1) was markedly attenuated by removal of Na+ or by exposure to H2DIDS, but secretion was not altered by acetazolamide (5 × 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-)n uptake across the basolateral membrane.Key words: duodenum, duodenal mucosa, bicarbonate ion, ion transport, amphibian, acetazolamide, sodium-bicarbonate cotransport, chloride-bicarbonate exchange.
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