The role of CFTR in bicarbonate secretion by pancreatic duct and airway epithelia

Abstract

The secretory epithelia of the pancreatic duct and airway share the ability to generate HCO(3)(-)-rich fluids. They both express CFTR (cystic fibrosis transmembrane conductance regulator) at the apical membrane and both are adversely affected by cystic fibrosis. CFTR is predominantly a Cl(-) channel, and it is widely believed that HCO(3)(-) secretion in the pancreatic duct is mediated mainly by a Cl(-)/HCO(3)(-) exchanger at the apical membrane. Studies on airway epithelia, however, have suggested that CFTR, despite its low permeability to HCO(3)(-), may nonetheless be directly responsible for HCO(3)(-) secretion across the apical membrane. This article reviews recent work that has re-examined both of these hypotheses.