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Regulation of Cl−/HCO3− Exchange in the Lower Villous Epithelium of Murine Duodenum

Previous studies of duodenal lower villous epithelium revealed that Slc26a3 (Dra) was solely responsible for apical membrane Cl−/HCO3− exchange. These studies were performed using luminal glucose to lower intracellular pH for measurements with the pH‐sensitive dye BCECF. However, Na+‐coupled glucose transport also depolarizes the apical membrane and may minimize activity of Slc26a6 (Pat‐1) which is also expressed and reportedly has an electrogenic 1Cl−:2HCO3− stoichiometry. To investigate regulation of Cl−/HCO3− exchangers, the effects of luminal glucose and cAMP stimulation (to activate CFTR) on the rates of Cl−in/HCO3−out exchange in Pat‐1 knockout (KO), DraKO and wild‐type (WT) littermate mice were measured. In the absence of luminal glucose (replaced with mannose), Cl−/HCO3− exchange was reduced ~50% in both the Pat‐1KO and DraKO, as compared to WT. With luminal glucose, Cl−/HCO3− exchange was unaffected in the Pat‐1KO and abolished in the DraKO. cAMP stimulation reduced Cl−/HCO3− exchange by 50% in WT and DraKO villi, but had no effect on Pat‐1KO villi. We conclude that Dra and Pat‐1 contribute to basal Cl−/HCO3− exchange, whereas regulation by luminal glucose or cAMP stimulation reduces activity of Pat‐1 but not Dra in duodenal lower villous epithelium. These findings are consistent with electroneutral Dra and electrogenic Pat‐1 Cl−/HCO3− activities. Supported by NIH.