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Gastric luminal hydrogen ions, commonly referred to as gastric acid, are secreted by the parietal cells of the stomach lining via the H+/K+ ATPase pump [2]. These ions create a highly acidic environment (pH 1.5 to 3.5) essential for the denaturation of dietary proteins and the conversion of pepsinogen into the active proteolytic enzyme pepsin [2]. Beyond digestion, the acidic environment serves as a critical physiological barrier against ingested pathogens [2]. However, excessive accumulation or reflux of these ions into the esophagus can lead to mucosal damage, resulting in conditions such as gastroesophageal reflux disease (GERD) and peptic ulcers [4]. While many drugs like proton pump inhibitors (PPIs) and H2-receptor antagonists reduce the production of these ions, antacids act by directly neutralizing the existing luminal H+ through chemical reactions [1]. This neutralization provides rapid symptomatic relief by increasing the gastric pH and reducing the corrosive effect of the acid on the gastrointestinal mucosa [1, 3].
Direct chemical neutralization of gastric acid to increase luminal pH, thereby reducing the acidity of the gastric contents [1].
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