抄録
Pancreatic duct cells secrete HCO3− into HCO3−-rich luminal fluid. Candidate mechanisms for HCO3− transport across the apical membrane are HCO3− conductance of CFTR and Cl−/HCO3− exchange by SLC26 family of anion transporters. In this study, we examined net transport of HCO3− and Cl− in interlobular ducts isolated from guinea-pig pancreas. Luminal pH, Cl− concentration and volume were measured in ducts of which the lumen was injected with BCECF-dextran or ABQ-dextran. Duct lumen was first filled with HCO3−-free, Cl−-rich (150 mM) solution. When the superfusate was switched from HCO3−-free, Cl−-rich (150 mM) solution to the solution containing 25 mM HCO3−, 5% CO2, and 125 mM Cl−, luminal pH transiently decreased (due to CO2 diffusion) and then increased due to HCO3− secretion. Luminal Cl− quickly decreased to ∼90 mM in 2 min. Calculation of net Cl− flux indicated significant absorption of Cl− during the 2-min period, probably via apical Cl−/HCO3− exchange. Then we investigated the role of SLC26A6 in apical Cl−/HCO3− exchange using Slc26a6 null and wild-type (wt) mice. Apical Cl−/HCO3− exchange activity was estimated by measuring intracellular pH in microperfused interlobular ducts loaded with BCECF. The HCO3−-efflux mode of apical [Cl−]o/[HCO3−]i exchange was decreased in Slc26a6 null mice (p<0.05 vs wt), whereas the HCO3−-influx mode of apical [Cl−]i/[HCO3−]o exchange was increased in Slc26a6 null mice (p<0.01), suggesting the uni-directionality of the Slc26a6-mediated HCO3− transport. [J Physiol Sci. 2007;57 Suppl:S61]
