Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The simultaneous effects of acute i.v. ethanol administration (1.3 gm./kg.) on pancreatic and gastric acid secretion was studied on dogs provided with chronic pancreatic and gastric fistulas (Thomas cannula) and subjected to a continuous i.v. injection of GIH secretin (0.5 CU./kg./hr.) and gastrin (Eurorga hog gastrin I-II, 6 gamma/kg./hr.). Acute i.v. ethanol inhibits the pancreatic secretion of protein (concentration and output) and stimulates gastric acid secretion. Experiments were repeated: 1. Superimposing an atropine infusion (1.0 mg./hr.) on the continuous hormonal perfusion. 2. After reserpine administration for 48 hours (0.10 mg./kg./24 hr.) Atropine abolished the ethanol-mediated inhibition of pancreatic protein secretion but did not prevent the alcohol-mediated gastric acid stimulation. Reserpine did not change the ethanol-mediated pancreatic inhibition. It is assumed that in nonalcoholic dogs, i.v. ethanol inhibits pancreatic secretion by an intermediate nervous mechanism and enhances gastric acid secretion by acting directly on the oxyntic cells. Reserpine induces a high plateau level of HCl secretion which obscures the ethanol-mediated excitatory influences on the oxyntic cells.
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PMID:Simultaneous changes in pancreatic and gastric secretion induced by acute intravenous ethanol infusion. Effect of atropine and reserpine. 114 96

The histamine-storing ECL cells in the stomach play a key role in the control of acid secretion. They contain granules, secretory vesicles and microvesicles, and sustained gastrin stimulation results in the additional formation of vacuoles and lipofuscin bodies. The cells are rich in the vesicle monoamine transporter type-2 (VMAT-2), which can be inhibited by reserpine. The present study examines the effect of reserpine on ECL-cell ultrastructure and histamine compartmentalization. Rats received reserpine and/or gastrin. Reserpine was given twice by the intraperitoneal route (25 mg/kg once daily). Gastrin-17 was given by subcutaneous infusion (5 nmol/kg/h), starting at the time of the first reserpine injection and continuing for 4 days when the rats were killed. At this stage, histamine in the oxyntic mucosa was unaffected by reserpine but elevated by gastrin. Immunocytochemical analysis (confocal microscopy) showed ECL-cell histamine in control and gastrin-treated rats to be localized in cytoplasmic organelles (e.g., secretory vesicles). After treatment with reserpine alone or reserpine+gastrin, ECL-cell histamine occurred mainly in the cytosol. Planimetric analysis (electron microscopy) of ECL cells showed reserpine to increase the number, size and volume density of the granules and to reduce the size and volume density of the secretory vesicles. Gastrin reduced the number and volume density of granules and secretory vesicles, increased the number and volume density of microvesicles and caused vacuoles and lipofuscin bodies to appear. Reserpine+gastrin increased the number, volume density and size of the granules. Reserpine prevented the effects of gastrin on secretory vesicles, vacuoles and microvesicles, but did not prevent the development of lipofuscin. Our findings are in line with the views: (1) that preformed cytosolic histamine is taken up by granules/secretory vesicles via VMAT-2, that histamine is instrumental in the transformation of granules into secretory vesicles and in their consequent enlargement and (2) that vacuoles are formed by the fusion of large secretory vesicles.
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PMID:Effects of reserpine on ECL-cell ultrastructure and histamine compartmentalization in the rat stomach. 993 59