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Gastric acid, primarily hydrochloric acid (HCl), is secreted by parietal cells of the stomach and is the main acidic component in gastric juice. Its low pH (1–3) is crucial for activating digestive enzymes (notably, the conversion of pepsinogen to pepsin), aiding in the digestion of proteins and absorption of certain nutrients and minerals, and acting as an antimicrobial barrier to prevent pathogens from reaching the intestines. Acid secretion is regulated by neural (vagus nerve), hormonal (gastrin, somatostatin), and paracrine (histamine) mechanisms. While essential for normal gastrointestinal function, imbalances in free gastric acid—either excess (hyperchlorhydria) or deficiency (hypochlorhydria)—are implicated in a range of diseases such as peptic ulcers, gastritis, and increased susceptibility to gastrointestinal infections. Pharmacological agents frequently target the acid secretion process itself, not the acid as a molecule[1][2][3][4][5][6][7]. Note: "Free gastric acid" is not a therapeutic target or druggable protein/receptor, making it an incorrect entry as a target. It refers to a measurable chemical/physiological property, not a molecule amenable to direct modulation by drugs as a receptor or enzyme is.
Drugs reduce gastric acid secretion by inhibiting H+/K+ ATPase (proton pump inhibitors), blocking H2 receptors on parietal cells (H2RAs), or neutralizing the acid (antacids)[3].
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