The glands of the stomach typically secrete ~2 L/day of a fluid that is
approximately isotonic with blood plasma. Consequence of the heterogeneity of gastric mucosal function, early investigators recognized that gastric secretion consists of two distinct components: 1. Parietal cell- stimulated component that represents secretion that is rich in H+ 2. Non-parietal has Na+ -rich basal secretion This model helps to explain the inverse relationship between the luminal concentrations of H+ and Na+ as a function of the rate of gastric secretion At high rates of gastric secretion—for example, when gastrin or histamine stimulates parietal cells—intraluminal [H+ ] is high, whereas intraluminal [Na+ ] is relatively low. At low rates of secretion or in clinical situations in which maximal acid secretion is reduced (e.g., pernicious anemia) intraluminal [H+ ] is low but intraluminal [Na+ ] is high. The proximal portion of the stomach secretes acid, pepsinogens, intrinsic factor, bicarbonate the distal part releases gastrin and somatostatin The body of the stomach contains oxyntic glands that empty their secretory products, via ducts, into the lumen of the stomach The openings of the ducts on the gastric mucosa are called pits, which are lined with epithelial cells. Deeper in the gland are mucous neck cells, parietal (oxyntic) cells, and chief (peptic) cells. The parietal cells have two secretory products, HCl and intrinsic factor. The chief cells secrete pepsinogen. The antrum of the stomach contains the pyloric glands The pyloric glands contain two cell types: the mucous cells and the endocrine cells include the so-called G cells and D cells The G cells secrete gastrin, not into the pyloric ducts but into the circulation. D cells secrete somatostatin The mucous neck cells secrete mucus, HCO3 and pepsinogen. Mucus and HCO3 have a protective, neutralizing effect on the gastric mucosa. An H-K pump is responsible for gastric acid secretion by parietal cells acetylcholine (ACh), gastrin, and histamine bind directly to membrane receptors on the parietal cell and stimulate and potentiate acid secretion. ACh is released from endings of the vagus nerve Gastrin is released by both antral and duodenal G cell These G cells release gastrin in response to luminal peptides and amino acids, as well as in response to gastrin releasing peptide (GRP) that is released by vagal nerve endings Gastrin release is inhibited by somatostatin, Somatostatin is also made by the δ cells of the pancreatic islets and by neurons in the hypothalamus Histamine is synthesized from histidine histamine is released by entero chromaffin-like cells in the corpus ACh and gastrin indirectly induce acid secretion as a result of their stimulation of histamine release from ECL cells in the lamina propria