Summary

Patients with cystic fibrosis demonstrate a defect in HCO3- secretion by their pancreatic duct cells. However, attempts toward understanding or correcting this defect have been hampered by a lack of knowledge regarding the cellular and molecular mechanisms mediating HCO3- transport in these cells. Recent functional and molecular studies indicate a major role for a basolateral electrogenically-driven Na+:HCO3-cotransporter (NBC1) in mediating the transport of HCO3- into the duct cells. The HCO3- exits at the lumen predominantly via two recently discovered apical HCO3-transporters. cAMP, which mediates th