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Bicarbonate secretion in the gastric epithelium is a physiological defense mechanism whereby surface epithelial cells transport bicarbonate ions into the mucus layer covering the stomach lining. This is primarily mediated by transporters such as anion exchanger 2 (AE2/SLC4A2) and sodium bicarbonate cotransporter 1 (NBCe1/SLC4A4). These molecules orchestrate the exchange of bicarbonate and chloride (or sodium) ions, maintaining a near-neutral pH at the epithelial surface and protecting against acid and pepsin-induced damage. Impaired bicarbonate secretion is implicated in several gastric diseases, and pharmacologic agents that modulate this pathway can have therapeutic or adverse effects.
Inhibitors block ion exchange or cotransport activity, reducing bicarbonate secretion and altering local pH protection Some agents (e.g., prostaglandins, VIP) stimulate bicarbonate secretion via signaling pathways
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