MECHANISMS OF BICARBONATE SECRETION IN THE PANCREATIC DUCT

Abstract

▪ Abstract In many species the pancreatic duct epithelium secretes HCO3− ions at a concentration of around 140 mM by a mechanism that is only partially understood. We know that HCO3− uptake at the basolateral membrane is achieved by Na+-HCO3− cotransport and also by a H+-ATPase and Na+/H+ exchanger operating together with carbonic anhydrase. At the apical membrane, the secretion of moderate concentrations of HCO3− can be explained by the parallel activity of a Cl−/HCO3− exchanger and a Cl− conductance, either the cystic fibrosis transmembrane conductance regulator (CFTR) or a Ca2+-activated Cl− channel (CaCC). However, the sustained secretion of HCO3− into a HCO3−-rich luminal fluid cannot be explained by conventional Cl−/HCO3− exchange. HCO3− efflux across the apical membrane is an electrogenic process that is facilitated by the depletion of intracellular Cl−, but it remains to be seen whether it is mediated predominantly by CFTR or by an electrogenic SLC26 anion exchanger.