Cl(-)-dependent HCO3- transport by cystic fibrosis transmembrane conductance regulator.
Cystic fibrosis (CF) affects the function of multiple organs. The inability to maintain luminal hydration of ducts leads to their plugging and destruction of the affected organs. An exacerbating problem is the acidic pH of the fluid produced by CF patients' secretory glands. This is best documented for pancreatic secretion. Alkaline fluid secretion requires vectorial transport of electrolytes and of HCO(3)(-). The mechanism of HCO(3)(-) secretion by cystic fibrosis transmembrane conductance regulator (CFTR) expressing cells is not well understood. In the present communication we discuss results suggesting that CFTR itself can transport large amounts of HCO(3)(-) and that HCO(3)(-) transport by CFTR is mediated by a coupled, Cl(-)-dependent process that is different from a simple HCO(3)(-) conductance.
Choi
J Y
JY
Department of Physiology, UT Southwestern Medical Center, Dallas, TX 75235-9040, USA. smuall@mednet.swmed.edu
Lee
M G
MG
Ko
S
S
Muallem
S
S
D027963:Chloride-Bicarbonate Antiporters / Q000378:metabolism* / Q000502:physiology; D002712:Chlorides / Q000378:metabolism*; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000502:physiology*; D006801:Humans
C505032:CFTR protein, human; D027963:Chloride-Bicarbonate Antiporters; D002712:Chlorides; D019005:Cystic Fibrosis Transmembrane Conductance Regulator