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)

In the present study we have analyzed if cholecystokinin (CCK) or gastrin (G) can inhibit acid production in isolated rabbit gastric glands as revealed by the aminopyrine technique. The results show that G 17 I, CCK 8 NS, CCK 8 S, ceruletide and CCK 39 significantly inhibit histamine induced aminopyrine accumulation. No significant inhibition was noted for G 4, G 34 and NT G 1-13. As a group the CCK peptides were more effective than the gastrin peptides in inhibiting the aminopyrine uptake. CCK 8 S and ceruletide, the most potent inhibitors, reduced histamine induced aminopyrine accumulation with an ED50 of 10(-9) and 10(-10) M respectively. These potencies are similar to those by which CCK peptides stimulate isolated pancreatic acini to secrete amylase. Inhibition evoked by CCK 8 S was most effective following 20-40 min of incubation time, possibly indicating that the effect is mediated by the release of an intermediate substance. The results may therefore indicate a role for cholecystokinin as a physiological inhibitor of acid secretion in the rabbit. The results may also contribute to explain why the potent gastric secretagogue gastrin per se fails to stimulate acid formation in gastric glands isolated from the rabbit.
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PMID:Cholecystokinin and gastrin inhibit histamine stimulated aminopyrine uptake in isolated rabbit gastric glands. 276 88

A bioassay sensitive to gastrin (G 1-17) in physiological concentrations and suitable for testing of biological activity of minor amounts of radioiodinated gastrin is reported. G 1-17 was iodinated by a gentle Iodo-gen method and purified to high specific activity (1900 Ci/mmol). Totally isolated vascularly perfused rat stomachs were prepared and stimulated by graded amounts of G 1-17. Gastrin 'dose'-dependently increased the acid output from 5.7 +/- 1.0 mueq/40 min (basal) to a maximum of 58.8 +/- 10.0 mueq/40 min at a concentration of 520 pmol/l in the vascular perfusate. The lowest G 1-17 concentration that significantly increased the acid output from the basal value was 65 pmol/l, corresponding to a dose of 17.5 ng/stomach-hour. 125I-G 1-17 also increased the acid output significantly at this threshold dose. The amount of lactic acid enzymatically determined in the luminal perfusate was negligible, indicating a true parietal cell stimulation. Accordingly, a very sensitive bioassay for gastrin, suitable for testing of biological activity of G 1-17 and 125I-G, is described. Significant acid responses were obtained with physiological concentrations of gastrin, requiring less than 100 ng of hormone and labelled hormone, respectively, to show biological activity.
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PMID:Bioassay of gastrin, using the totally isolated, vascularly perfused rat stomach. A biomodel sensitive to gastrin in physiological concentrations. 377 61