Gastrins

Bombesin Intestinal mucosa Mechanism of release unknown stimulates gastric and pancreatic secretions directly and by release of gastrin and CCK, respectively inhibits absorption of water, Na , and CI from the jejunum. [Pg.203]

Bulbogastrone Mucosa of duodenal bulb Released by acid inhibits gastric secretion. [Pg.203]

Enteroglucagon Duodenal mucosa Functions like glucagon (Chapter 22). [Pg.203]

Motilin Duodenum and jejunum Released by vagal stimulation and passage of nutrients modulates interdigestive motility, clearing the intestine between meals and preparing it for another nutritional bolus. [Pg.203]

Somatostatin Intestinal mucosa, pancreas and nerves hypothalamus Mechanism of release not clear multiple inhibitory actions. [Pg.203]

Gas solubility Gas sweetening Gas-treating Gastric acid Gastric prokinetics Gastrin... [Pg.435]

Two CCK receptor subtypes, CCK and CCKg are known. A related receptor, the gastrin receptor, has also been described. CCK receptors predominate in the gastrointestinal tract and pancreas and are also localized in discrete brain regions. CCKg receptors predominate in the brain. A 71623... [Pg.538]

The histamine H2-receptor (359 amino acids) is best known for its effect on gastric acid secretion. Histamine H2-receptor activation, in conjunction with gastrin and acetylcholine from the vagus, potently stimulate acid secretion from parietal cells. High concentrations of histamine are also present in cardiac tissues and can stimulate positive chronotropic and inotropic effects via H2-receptor stimulation and activation of adenylyl... [Pg.589]

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). [Pg.1483]

Gastrin Releasing Peptide Gastroesophageal Reflux Disease (GERD)... [Pg.1492]

Interaction of the food with the gastric mucosal layer is the normal trigger for gastric cells to release gastrin, which is then carried by the bloodstream to the parietal cells. Calcium ions and cyclic AMP act as intracellular messengers in the transfer of the signal from the receptors to the proton pumps of parietal cells where the acid is generated. [Pg.49]

IC5Q — 3.4 pM gastrin-releasing peptide/bombesin receptor... [Pg.7]

L. J. Holtermuller, K. H. Arnaud, C. D. "Relations of Calcitonin and Gastrin in the Zollinger-Ellison Syndrome and Medullary Carcinoma of the Thyroid". N. Engl. J. Med. [Pg.55]

TEMLER R s, METTRAUX c (1986) Gastrin and cholecystokinin levels in rats fed soya bean trypsin inhihitor. Adv Exp Med Biol. 199 133—41. [Pg.185]

MAJUMDAR A p (1990) Role of tyrosine kinases in gastrin induction of ornithine decarboxylase in colonic mucosa. Am J Physiol. 259 (4 Ptl) G626-G630. [Pg.217]

Glycine-atginine-glycine-aspartic acid serine-proline Gro Growth-related oncogene GRP Gastrin-related peptide Gs Stimulatory G protein GSH Glutathione (reduced)... [Pg.282]

Less common causes of peptic ulceration include Zollinger-Ellison syndrome (ZES), cancer chemotherapy, radiation, and vascular insufficiency. ZES is caused by a gastrin-producing tumor called a gastrinoma and results in gastric acid hypersecretion. High-dose oral proton pump inhibitor (PPI) therapy is the initial treatment of choice for ZES intermittent intravenous PPI therapy may be required for any patient in whom oral therapy is contraindicated.1... [Pg.270]

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