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Bicarbonate secretion in the gastric mucosa is the active process by which surface epithelial cells of the stomach secrete bicarbonate ions (HCO₃⁻) into the adherent mucus layer, creating a near-neutral pH microenvironment to protect the epithelium from gastric acid and pepsin. This process relies on transporters like Na+/HCO₃− cotransporters (NBC1/NBC2) and Cl−/HCO₃− exchanger (AE4/SLC4), and the enzyme carbonic anhydrase. It is stimulated by cholinergic agonists, prostaglandins E-class, VIP, and low luminal pH, while inhibited by atropine, metabolic inhibitors, acetazolamide, NSAIDs, aspirin, and cigarette smoke. Impairment increases the risk of gastritis and peptic ulcer disease.
Modulation of bicarbonate transport via alteration of transporters (Na+/HCO₃− cotransporters NBC1/NBC2; Cl−/HCO₃− exchanger AE4/SLC4) and/or carbonic anhydrase activity
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