Proton Pump Inhibitors Inhibit Pancreatic Secretion: Role of Gastric and Non-Gastric H+/K+-ATPases

摘要: The mechanism by which pancreas secretes high HCO3- has not been fully resolved. This alkaline secretion, formed in pancreatic ducts, can be achieved transporting from serosa to mucosa or moving H+ the opposite direction. aim of present study was determine whether H+/K+-ATPases are expressed and functional human ducts proton pump inhibitors (PPIs) have effect on those. Here we show that gastric HKα1 HKβ subunits (ATP4A; ATP4B) non-gastric HKα2 (ATP12A) cells. Pumps similar localizations duct cell monolayers (Capan-1) pancreas, notably pumps localized luminal membranes. In Capan-1 cells, PPIs inhibited recovery intracellular pH acidosis. Furthermore, rats treated with PPIs, secretion but concentrations major ions follow excretory curves control PPI animals. addition HCO3-, also K+. conclusion, this calls for a revision basic model secretion. We propose transport is driving it may provide protective buffer zone K+ recirculation. seems relevant re-evaluate should used treatment therapies where functions already compromised.