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Cystic fibrosis transmembrane conductance regulator currents in guinea pig pancreatic duct cells: Inhibition by bicarbonate ions

Publication Date
DOI: 10.1016/s0016-5085(00)70372-6
  • Biology
  • Pharmacology


Abstract Background & Aims: Cystic fibrosis transmembrane conductance regulator (CFTR) Cl − channels play an important role in HCO 3 − secretion by pancreatic duct cells (PDCs). Our aims were to characterize the CFTR conductance of guinea pig PDCs and to establish whether CFTR is regulated by HCO 3 −. Methods: PDCs were isolated from small intralobular and interlobular ducts, and their Cl − conductance was studied using the whole-cell patch clamp technique. Results: Activation of a typical CFTR conductance by adenosine 3',5'-cyclic monophosphate (cAMP) was observed in 114 of 204 cells (56%). A larger (10-fold), time- and voltage-dependent Cl − conductance was activated in 39 of 204 cells (19%). Secretin had a similar effect. Coexpression of both conductances in the same cell was observed, and both conductances had similar anion selectivity and pharmacology. Extracellular HCO 3 − caused a dose-dependent inhibition of both currents ( K i, ̃7 mmol/L), which was independent of intracellular and extracellular pH, and the PCO 2 and CO 3 2− content of the bathing solutions. Conclusions Two kinetically distinct Cl − conductances are activated by cAMP in guinea pig PDCs. Because these conductances are coexpressed and exhibit similar characteristics (anion selectivity, pharmacology, and HCO 3 − inhibition), we conclude that CFTR underlies them both. The inhibition of CFTR by HCO 3 − has implications for the current model of pancreatic ductal HCO 3 − secretion. GASTROENTEROLOGY 2000;118:1187-1196

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