Gastric phase of gastric acid secretion is influenced by
Correct Answer: Gastrin
Description: The gastric secretions arise from glands in the wall of the stomach that drain into its lumen, and also from the surface cells that secrete primarily mucus and bicarbonate to protect the stomach from digesting itself, as well as substances known as trefoil peptides that stabilize the mucus-bicarbonate layer. The glandular secretions of the stomach differ in different regions of the organ. The most characteristic secretions derive from the glands in the fundus or body of the stomach. There are three primary stimuli of gastric secretion, each with a specific role to play in matching the rate of secretion to functional requirements. Gastrin is a hormonethat is released by G cells in the antrum of the stomach both in response to a specific neurotransmitter released from enteric nerve endings, known as gastrin-releasing peptide (GRP, or bombesin) and also in response to the presence of oligopeptides in the gastric lumen. Gastrin is then carried through the bloodstream to the fundic glands, where it binds to receptors not only on parietal (and likely, chief cells) to activate secretion but also on so-called enterochromaffin-like cells (ECL cells) that are located in the gland and release histamine. Histamine is also a trigger of parietal cell secretion, binding to H2 histamine receptors. Finally, parietal and chief cells can also be stimulated by acetylcholine, released from enteric nerve endings in the fundus. During the cephalic phase of gastric secretion, secretion ispredominantly activated by vagal input that originates from the brain region known as the dorsal vagal complex, which coordinates input from higher centers. Vagal outflow to the stomach then releases GRP and acetylcholine, thereby initiating secretory function. However, before the meal enters the stomach, there are few additional triggers and thus the amount of secretion is limited. Once the meal is swallowed, on the other hand, meal constituents trigger substantial release of gastrin and the physical presence of the meal also distends the stomach and activates stretch receptors, which provoke a "vago-vagal" as well as local reflexes that fuher amplify secretion. The presence of the meal also buffers gastric acidity that would otherwise serve as a feedback inhibitory signal to shut off secretion secondary to the release of somatostatin, which inhibits both G and ECL cells as well as secretion by parietal cells themselves. This probably represents a key mechanism whereby gastric secretion.REF: GANONG&;S REVIEW OF MEDICAL PHYSIOLOGY, KIM BARRETT, SCOTT BOITANO, SUSAN BARMAN, HEDDWEN BROOKSTWENTY THIRD EDITIONPAGE NO: 432,433
Category:
Physiology
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