Stomach gastrin

Zollinger-Ellison syndrome (ZES) is characterized by the development of a tumor (gastrinoma) or tumors that secrete excessive levels of gastrin, a hormone that stimulates production of acid by the stomach. In most cases, the tumor or tumors arise within the pancreas and/or the upper region of the small intestine (duodenum). 

Antrectomy Surgical excision of the wall of the antrum, the region of the stomach that produces the hormone gastrin. 

Gastrin G cells in pyloric region of the stomach Protein in stomach vagal stimulation Stimulates parietal cells (HC1) and chief cells (pepsinogen) in stomach enhances gastric motility... 

The major gastric factor that affects motility and the rate of emptying is the volume of chyme in the stomach. As the volume of chyme increases, the wall of the stomach becomes distended and mechanoreceptors are stimulated. This elicits reflexes that enhance gastric motility by way of the intrinsic and vagus nerves. The release of the hormone gastrin from the antral region of the stomach further contributes to enhanced motility. 

Gastrin is a hormone produced by gastric endocrine tissue — specifically, the G cells in the pyloric gland area. It is released into the blood and carried back to the stomach. The major function of gastrin is to enhance acid secretion by directly stimulating parietal cells (HC1) and chief cells (pepsinogen). Gastrin also stimulates the local release of histamine from enterochromaf-fin-like cells in the wall of the stomach. Histamine stimulates parietal cells to release HC1. 

The gastric phase is elicited by the presence of food in the stomach. Distension of the stomach wall, as well as the presence of protein, caffeine, and alcohol, enhances gastric secretion. This phase is mediated by the intrinsic nerves, the vagus nerve, and gastrin. Each of these mechanisms promotes secretion of HC1 and pepsinogen. 

Gastrin A hormone released after eating. Gastrin causes the stomach to produce more acid. [NIH]... 

The basal rate of proton secretion is around 10% of maximal but the perception of food (smell, taste, sight or even just the thought of it) increases secretion. This is the cephalic effect of food. Nervons signals from the brain canse release of acetylcholine, histamine and gastrin to stimnlate acid secretion from the parietal cells. When food actnally reaches the stomach, distension, proteins, peptides and amino acids farther stimulate the release of gastrin. 

Prostaglandins inhibit the secretion of protons by the parietal cells in the stomach, which is normally increased in response to food and the hormone gastrin. Consequently, inhibition of prostaglandin synthesis by aspirin or other similar drugs results in increased secretion of protons by the stomach, which can result in considerable gastric discomfort and can, if chronic, lead to the development of a peptic ulcer. Consequently, there is some conflict between the use of such inhibitors to relieve chronic pain (see below), in diseases such as arthritis, and the risk of development of ulcers. 

Cimetidine is a representative of first-generation antihistamine drugs that block H2 receptors. The main pharmacological effect of cimetidine is the suppression of gastric juice secretion associated with H2 receptors of the stomach walls. It suppresses both basal and stimulated hyckochloric acid produced by food as well as histamine and gastrine, which simultaneously lower pepsin activity. 

Ranitidine is a second-generation H2-receptor-blocking drug. Like cimetidine, ranitidine suppresses both basal and stimulated hydrochloric acid produced by food, histamine, gastrin, and acetylcholine. It simultaneously reduces pepsin activity and is used for treating stomach and duodenum ulcers as well as other conditions accompanied by elevated acidity of the gastrointestinal tract. Synonyms of this drag are zantac, azantac, raniplex, ranidil, and others. 

A. Gastrin, histamine, and acetylchohne stimulate gastric acid secretion. Pepsin is a digestive protein secreted by the stomach in response to a meal. Norepinephrine is a neurotransmitter that does not affect gastric acid secretion. 

Gastrin Polypeptide (17 residues) Stimulates acid secretion from stomach and pancreatic secretion... 

Bado, A., Moizo, L., Laigneau, J.P., Delwaide, J., Lewin, M.J.M., 1994. H3-receptor regulation of vascular gastrin and somatostatin releases by the isolated rat stomach. Yale J. Biol. Med. 67, 113-121. 

Bunnett, N.W., et al. 1988. Isolation of endopeptidase-24.11 (EC 3.4.24.11, enkephalinase ) from the pig stomach. Hydrolysis of substance P, gastrin-releasing peptide 10, [Leu5] enkephalin, and [Met5] enkephalin. Gastroenterology 95 952. 

It is likely that the hormone gastrin, which is secreted by the stomach antral mucosa in response to distension, also plays some role in this effect because gastrin has an excitatory effect on the colon and an inhibitory effect on the ileocecal valve, thus allowing rapid emptying of ileal contents into the cecum. This in turn elicits increased colonic activity. 

Gastrin (peptide) Stomach Lining Stomach release from pancreas and liver, contractions of gall bladder Stimulates stomach movement and... 

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