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 purpose of the present series of tests was to measure and compare the effects of ingestion of gelatin capsules containing 15(R)-15-methyl PGE2 (PG) and/or an anticholinergic drug (methscopolamine bromide, Pamine) on meal-induced gastric acid secretion and serum gastrin level. Eleven duodenal ulcer patients were stimulated by a 5% peptone meal. Acid secretion was determined by the intragastric titration technique, and serum gastrin was measured by radioimmunoassay. The tests were randomized and double-blind. PG alone given 30 min before a test meal at a dose of 50 micrograms or 100 micrograms produced no side effects and inhibited meal-stimulated acid secretion by about 43% and 55%, respectively. Gastric acid inhibition after a single dose of PG was most pronounced in the first hour of a test meal and was accompanied by almost complete suppression of the meal-induced serum gastrin level. Pamine alone in a dose of 2.5 mg reduced gastric acid response to a meal by about 29% but caused a further rise of postprandial serum gastrin level over control values. The combination of PG, 50 micrograms, and Pamine, 2.5 mg, did not result in significantly greater acid inhibition (about 48%) than when either compound was given alone. When the higher dose of PG (100 micrograms) was given together with Pamine (2.5 mg), the degree of inhibition produced by PG alone was not changed. It is concluded that PG given orally in capsules is a potent inhibitor of gastric acid and serum gastrin response to a meal and that this effect may be of potential value in the treatment of peptic ulcer disease.
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PMID:Effect of orally administered 15(R)-15-methyl prostaglandin E2 and/or an anticholinergic drug on meal-induced gastric acid secretion and serum gastrin level in patients with duodenal ulcers. 39 27

Previous reports on the profile of lower oesophageal sphincter (LOS) pressures and swallow responses in achalasia have been conflicting. Both normal and high resting pressures have been reported. Many reports have noted a failure of relaxation of the LOS in response to swallowing. Manometric studies were performed on 17 untreated patients with achalasia, of whom 76% were found to have a resting peak end-inspiratory pressure significantly greater than normal (P = 0,001). Nine patients showed relaxation of the LOS in response to swallowing but this relaxation was usually inadequate and of brief duration. Contractions were premature in 16 patients. One patient showed a manometric pattern closely simulating a Mobitz type 1 atrioventricular block in response to repeated swallows. A common pathophysiological process is postulated. In one patient an injection of secretin reduced the high resting LOS pressure. This supports previous evidence that a hypersensitive sphincter in achalasia is due to a hypersensitivity to gastrin. Hyoscine-N-butylbromide (Buscopan) caused a significant reduction in LOS pressure in all patients in whom it was used.
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PMID:Lower oesophageal sphincter resting pressures in achalasia and the response of the sphincter to swallowing and drugs. 99 80

The effect of dopamine (DA) on acid secretion was studied using the everted preparation of isolated rat stomachs. DA concentrations, measured by HPLC-ECD in the rumen, corpus and antrum were 1.06 nmol/mg protein, 0.49 nmol/mg protein and 2.92 nmol/mg protein, respectively. DA stimulated acid secretion at a concentration of 10 nM and elicited the maximum response at 10 microM, which was at a level approximately 1.56-fold that of the spontaneous secretion but only about half that of secretion induced by histamine at a concentration of 0.3 mM. The concentration-dependent stimulation by DA was antagonized by octopamine and SCH 23390. Failure of proglumide and cimetidine to affect this stimulation ruled out the participation of histamine and/or gastrin. Scopolamine and tetrodotoxin completely inhibited the acid secretion induced by low concentrations of DA but inhibited only partially the response induced by high concentrations of DA. The results obtained indicate that DA induces acid secretion via activation of the dopamine D1 receptor, located on the cholinergic neurons and on some nonneuronal cells, in the rat stomach.
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PMID:Stimulatory effect of dopamine on acid secretion from the isolated rat stomach. 775 4