EN
Proximal portion of duodenum is exposed to intermittent pulses of gastric H+ discharged by the stomach. This review summarizes the mechanisms of duodenal mucosal integrity, mainly the role of mucus-alkaline secretion and the mucous barrier protecting surface epithelium against gastric H+. The mucous barrier protects the leaky duodenal epithelium against each pulse of gastric H+, which penetrates this barrier and diffuses into duodenocytes, but fails to damage them due to; a) an enhanced expression of cyclooxygenase-1 (COX-1), with release of protective prostaglandins (PG) and of nitric oxide (NO) synthase (NOS) with, however, production of NO, stimulating duodenal HCO3- secretion and b) the release of several neurotransmitters also stimulating HCO3- secretion such as vasoactive intestimal peptide (VIP), pituitary adenylate-cyclase activating polypeptide (PACAP), acetylcholine, melatonin, leptin and ghrelin released by enteric nerves and mucosal cells. At the apical duodenocyte membrane at least two HCO3-/Cl- anion exchangers operate in response to luminal H+ to provide adequate extrusion of HCO3- into duodenal lumen. In the basolateral portion of duodenocyte membrane, both non-electrogenic (NBC) and electrogenic (NBCn) Na+-HCO3- cotransporters are activated by the exposure to duodenal acidification, causing inward movement of HCO3- from extracellular fluid to duodenocytes. There are also at least three Na+/H+ (NHE1-3) amiloride-sensitive exchangers, eliminating H+ which diffused into these cells. The Helicobacter pylori (Hp) infection and gastric metaplasia in the duodenum with bacterium inoculating metaplastic mucosa and inhibiting HCO3- secretion by its endogenous inhibitor, asymetric dimethyl arginine (ADMA), may result in duodenal ulcerogenesis.