Gastric secretion

Purpose of review The review summarizes the past year's literature regarding the regulation of gastric exocrine and endocrine secretion, both basic science and clinical. Recent findings Gastric acid secretion is an elaborate and dynamic process that is regulated by neural (efferent and afferent), hormonal (e.g. gastrin), and paracrine (e.g. histamine, ghrelin, somatostatin) pathways as well as mechanical (e.g. distension) and chemical (e.g. amino acids) stimuli. Secretion of hydrochloric acid (HCl) by parietal cells involves translocation of H+K+-ATPase-containing cytoplasmic tubulovesicles to the apical membrane with subsequent electroneutral transport of hydronium ions in exchange for potassium. The main apical potassium channel is KCNQ1 which, when activated, assembles with its beta-subunit KCNE2 to function as a constitutively open, voltage-insensitive, and acid-resistant luminal potassium channel. Proton pump inhibitors block acid secretion by covalently binding to cysteine residues accessible from the luminal surface of the H+K+-ATPase. Potassium-competitive ATPase blockers (P-CABs) act by competing for K+ on the luminal surface of H+K+-ATPase. As they are acid-stable and do not require acid-dependent activation, P-CABs hold promise for rapid and prolonged inhibition of acid secretion. Summary We continue to make progress in our understanding of the physiologic regulation of gastric acid secretion. A better understanding of the pathways and mechanisms regulating acid secretion should lead to improved management of patients with acid-induced disorders.