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Effect of Slc26a6 deletion on apical Cl^–/HCO₃^– exchanger activity and cAMP-stimulated bicarbonate secretion in pancreatic duct

¹Laboratory of Human Nutrition, Nagoya University Graduate School of Medicine, Nagoya, Japan; ²Department of Pharmacology, Institute of Gastroenterology, Yonsei University College of Medicine, Seoul, Korea; and Departments of ³Medicine and ⁴Surgery, University of Cincinnati and ⁵Veterans Administration Medical Center, Cincinnati, Ohio

Submitted 30 June 2006 ; accepted in final form 8 August 2006

ABSTRACT

The role of Slc26a6 (PAT1) on apical Cl^–/HCO₃^– exchange and bicarbonate secretion in pancreatic duct cells was investigated using Slc26a6 null and wild-type (WT) mice. Apical Cl^–/HCO₃^– exchange activity was measured with the pH-sensitive dye BCECF in microperfused interlobular ducts. The HCO₃^–-influx mode of apical [Cl^–]_i/[HCO₃^–]_o exchange (where brackets denote concentration and subscripts i and o denote intra- and extracellular, respectively) was dramatically upregulated in Slc26a6 null mice (P < 0.01 vs. WT), whereas the HCO₃^–-efflux mode of apical [Cl^–]_o/[HCO₃^–]_i exchange was decreased in Slc26a6 null mice (P < 0.05 vs. WT), suggesting the unidirectionality of the Slc26a6-mediated HCO₃^– transport. Fluid secretory rate in interlobular ducts were comparable in WT and Slc26a6 null mice (P > 0.05). In addition, when pancreatic juice was collected from whole animal in basal and secretin-stimulated conditions, neither juice volume nor its pH showed differences between WT and Slc26a6 null mice. Semiquantitative RT-PCR demonstrated more than fivefold upregulation in Slc26a3 (DRA) expression in Slc26a6 knockout pancreas. In conclusion, these results point to the role of Slc26a6 in HCO₃^– efflux at the apical membrane and also suggest the presence of a robust Slc26a3 compensatory upregulation, which can replace the function of Slc26a6 in pancreatic ducts.

cystic fibrosis transmembrane regulator; cystic fibrosis; sodium bicarbonate exchanger; HCO₃^– secretion; HCO₃^– transporters; downregulated in adenoma; putative anion transporter 1

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