The origin of and subcellular mechanisms causing pancreatic bicarbonate secretion

Abstract

In recent years, there has been a rapid growth in knowledge about the subcellular mechanisms involved in pancreatic ductal secretion of bicarbonate. The mechanisms governing anion transport across the luminal membrane of duct cells have been well characterized. Evidence suggests that the cystic fibrosis transmembrane conductance regulator is a cyclic adenosine monophosphate-regulated Cl- conductance in the luminal membrane that plays a pivotal role in ductal bicarbonate secretion by recirculating the Cl- imported into duct cells through Cl(-)-HCO3- exchange. The mechanisms governing ion transfer across the basolateral plasma membrane of duct cells are less well defined. There is some evidence suggesting that secretin may cause exocytotic insertion of proton pumps into the basolateral plasma membrane. Once inserted into the plasma membrane, proton pumps could engage in primary active electrogenic H+ ion transport to interstitial tissue while secondary active HCO3- secretion occurs over the luminal membrane through Cl(-)-HCO3- exchangers coupled in parallel with the cystic fibrosis transmembrane conductance regulator. These and other subcellular phenomena related to ductal secretory function are reviewed.