The role of CFTR in bicarbonate secretion by pancreatic duct and airway epithelia.
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.
Faculty of Life Sciences, University of Manchester, Manchester, UK.
Dusik
D
Kim
Martin C
MC
Steward
D000818:Animals; D001639:Bicarbonates / Q000378:metabolism*; D001692:Biological Transport / Q000502:physiology; D002462:Cell Membrane / Q000502:physiology; D027963:Chloride-Bicarbonate Antiporters / Q000502:physiology; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000502:physiology*; D006801:Humans; D010183:Pancreatic Ducts / Q000166:cytology / Q000378:metabolism*; D020545:Respiratory Mucosa / Q000166:cytology / Q000378:metabolism*
D001639:Bicarbonates; D027963:Chloride-Bicarbonate Antiporters; D019005:Cystic Fibrosis Transmembrane Conductance Regulator