Gastrointestinal

Parietal cells secrete HCl. They are stimulated by acetylcholine (M3, vagal), gastrin (CCK-B), and histamine (H2); histamine is the dominant potentiator. Acid is generated by the H+/K+ ATPase on the apical (luminal) membrane.

Parietal cells secrete intrinsic factor, which binds vitamin B12 (cobalamin) to permit its absorption in the terminal ileum. Loss of parietal cells (e.g., autoimmune/chronic gastritis) causes pernicious anemia.

Chief cells secrete pepsinogen, the inactive zymogen. Gastric acid (low pH) cleaves pepsinogen to active pepsin, which begins protein digestion. Pepsin further activates more pepsinogen (autocatalysis).

G cells in the gastric antrum secrete gastrin, which stimulates acid secretion (mainly indirectly via histamine release from ECL cells) and promotes gastric mucosal growth. Gastrin is increased by stomach distension, amino acids/peptides, and vagal stimulation (via GRP); it is inhibited by low pH (somatostatin).

D cells secrete somatostatin, which inhibits gastric acid, gastrin, pepsinogen, and pancreatic/biliary secretion, and decreases insulin/glucagon. It is the body's universal 'off' signal. The analog octreotide is used for acromegaly, variceal bleeding, and secretory tumors.

CCK is released by I cells of the duodenum/jejunum in response to fatty acids and amino acids. It causes gallbladder contraction, relaxation of the sphincter of Oddi, pancreatic enzyme secretion, and decreased gastric emptying. It acts via vagal pathways for pancreatic effects.