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Gastric mucosa bicarbonate secretion is a fundamental physiological process where surface epithelial cells secrete bicarbonate ions into the adherent mucus layer, maintaining a near-neutral pH at the epithelial surface despite the acidic gastric lumen. This mucus-bicarbonate barrier serves as a primary defense mechanism against acid and pepsin, protecting the stomach from autodigestion and ulcer formation. The process is regulated by neural (vagal), hormonal (prostaglandins E2, vasoactive intestinal peptide), and local (luminal acid) cues. Impaired bicarbonate secretion, such as that induced by NSAID use or in certain forms of peptic ulcer disease, decreases mucosal resistance and predisposes to injury.
Prostaglandin analogues stimulate mucus and bicarbonate secretion enhancing mucosal protection. NSAIDs inhibit prostaglandin synthesis, leading to reduced bicarbonate/mucus secretion and increased acid damage.
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