Thanks to recent progress in availability of molecular and functional techniques it became possible to search for the basic molecular and cellular processes that mediate and control HCO3- and fluid secretion by the pancreatic duct. The coordinated action of various transporters on the luminal and basolateral membranes of polarized epithelial cells mediates the transepithelial HCO3- transport, which involves HCO3- absorption in the resting state and HCO3- secretion in the stimulated state. The overall process of HCO3- secretion can be divided into two steps. First, HCO3- in the blood enters the ductal epithelial cells across the basolateral membrane either by simple diffusion in the forms of CO2 and H2O or by the action of an Na+-coupled transporter, a Na+-HCO3- cotranporter (NBC) identified as pNBC1. Subsequently, the cells secrete HCO3- to the luminal space using at least two HCO3- exit mechanisms at the luminal membrane. One of the critical transporters needed for all forms of HCO3- secretion across the luminal membrane is the cystic fibrosis transmembrane conductance regulator (CFTR). In the resting state the pancreatic duct, and probably other HCO3- secretory epithelia, absorb HCO3-. Interestingly, CFTR also control this mechanism. In this review, we discuss recent progress in understanding epithelial HCO3- transport, in particular the nature of the luminal transporters and their regulation by CFTR.
Absorption ; Cystic Fibrosis Transmembrane Conductance Regulator ; Diffusion ; Epithelial Cells ; Membranes ; Pancreas ; Pancreatic Ducts ; Phenobarbital

No abstract available.
Calcium Signaling/physiology* ; Cell Polarity/physiology* ; Epithelial Cells/physiology* ; Epithelial Cells/cytology*

No abstract available.
1-Methyl-3-isobutylxanthine/pharmacology ; Ammonium Compounds/pharmacology ; Animal ; Biological Transport/physiology ; Biological Transport/drug effects ; Cell Membrane/metabolism ; Cyclic AMP/metabolism* ; Forskolin/pharmacology ; Guanidines/pharmacology ; Mice ; Mice, Knockout ; Pancreatic Ducts/metabolism* ; Phosphodiesterase Inhibitors/pharmacology ; Protons ; Sodium-Hydrogen Antiporter/metabolism* ; Sodium-Hydrogen Antiporter/genetics ; Sulfones/pharmacology