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)

Oral calcium carbonate (0-5 g, pH 9-4) increased serum gastrin and gastric acid output with slight but insignificant change in serum calcium. A similar rise in serum calcium during an intravenous infusion of calcium gluconate failed to increase serum gastrin and gastric acid output. Both intragastric calcium actions were abolished by acidification of the calcium carbonate solution (pH 1-0). The increase in serum gastrin and gastric acid output after intragastric calcium carbonate was not affected, however, by a simultaneous intraduodenal acid load. Equivalent neutralising doses of magnesium hydroxide (pH 9-4) did not increase serum gastrin and gastric acid output above basal levels, whereas antral acidification with 20 ml 0-1 N HCl resulted in a slight decrease in serum gastrin. Intraduodenal calcium carbonate (pH 3-0) also increased serum gastrin and gastric acid output, whereas an equivalent volume of intraduodenal saline (pH 3-0) had no effect. These findings indicate that calcium increases serum gastrin by local stimulation of antral and duodenal mucosa. They also suggest that the action of calcium on gastric secretion is partly mediated by gastrin.
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PMID:Calcium stimulation of gastrin and gastric acid secretion: effect of small doses of calcium carbonate. 87 25

Immunoreactive gastrin cells were demonstrated in the human antral and duodenal mucosa. No gastrin immunoreactivity was seen in pancreatic islets. Formaldehyde- or Bouin-fixed material was used throughout for immunohistochemistry. Antral and duodenal gastrin cells, as well as pancreatic A2-cells, displayed strong formaldehyde- ozone- and formaldehyde-HCl-induced fluorescence, whereas the pancreatic A1-cells (claimed to store gastrin) were nonfluorescent. In the fetus, gastrin cells appeared first in the duodenal mucosa (earliest stage examined, 11 weeks) and much later in the antrum. The fluorescence histochemical properties of the fetal gastrin cells were not different from the adult.
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PMID:Fluorescence histochemistry of the gastrin cell infetal and adult man. 109 86

Treatment with formaldehyde gas and HCl vapor, simultaneously or in sequence, induces fluorescence with indoles, including tryptophan residues of peptides, as is evident from studies on protein droplet models. Among cells that display intense formaldehyde-HCl-induced fluorescence are pancreatic exocrine cells, gastric chief cells, Paneth cells and enterochromaffin cells. Peptide hormone-producing cells that can be visualized by the formaldehyde-HCl treatment include gastrin cells and glucagon cells. The simultaneous procedure has proved superior to the sequential procedure. Simultaneous formaldehyde-HCl treatment appears to be a useful method for the demonstration of tryptophan residues of peptides and proteins. It seems more sensitive than previously described indole methods.
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PMID:Formaldehyde-hydrochloric acid treatment. A fluorescence histochemical method for the demonstration of tryptophan residues in peptides and proteins. 110 7

In four dogs with chronic pancreatic and gastric fistulas, dose-response studies of pancreatic bicarbonate and protein secretion were done with intravenous infusions of secretin, octapeptide of cholecystokinin (OP-CCK), and 2-deoxyglucose (2-DG). The pancreatic response to a meal and to duodenal perfusion of graded concentrations of HCl, sodium oleate, and tryptophan were also studied. These observations were repeated after division of both the hepatic and celiac vagal branches to produce extragastric vagotomy, and subsequently after transthoracic truncal vagotomy. The responses to secretin, OP-CCK, and to duodenal perfusion of HCl were either unaltered or only slightly decreased by either extragastric or truncal vagotomy. Basal pancreatic secretion and the responses to duodenal perfusion of oleate and tryptophan were markedly depressed by extragastric vagotomy. These findings indicate that tonic vagal activity contributes to basal pancreatic secretion but has little effect on the response of the pancreas to secretin or CCK or on the release of secretin from the intestine. The decreased pancreatic response to intestinally perfused oleate and tryptophan seen after extragastric vagotomy could be caused either by interruption of reflex paths between gut and pancreas or by interference with CCK release. Extragastric vagotomy reduced pancreatic responses to a meal and to 2-DG and subsequent truncal vagotomy caused still further reduction, possibly, at least in part, by depressing release of antral gastrin.
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PMID:Effect of extragastric and truncal vagotomy on pancreatic secretion in the dog. 113 May 17

Dogs were provided with oesophageal fistulae, fully innervated pouches of the fundic stomach and the duodenal bulb, and a gastric cannula. Gastric secretion was stimulated by sham feeding for 10 min. The bulbar pouches were perfused either with 0.9 per cent NaCl or with 0.1 N HCl. Plasma gastrin concentrations were determined by radioimmunoassay. Bulbar acidification effectively inhibited gastric acid secretion. Plasma gastrin responses were not suppressed. Instead, plasma gastrin concentrations were higher than in controls. The results show that the bulbar mechanism does not inhibit gastric acid secretion by reducing gastrin release.
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PMID:Increased plasma gastrin levels in connection with inhibition of gastric acid responses to sham feeding following bulbar perfusion with acid in dogs. 113 29

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

Three dogs were provided with Pavlov pouches. In two subsequent operations the antrum and the duodenal bulb were removed and the gastrointestinal continuity was restored by gastroduodenostomy. Gastric acid and gastrin secretion were stimulated by a test meal. The feeding experiments were repeated after each operation. The gastrin response to a test meal was markedly reduced but not eliminated by antral resection. Additional removal of the duodenal bulb significantly lowered the basal plasma gastrin concentration and abolished the gastrin response to feeding. The acid response to test meals was significantly increased by antrectomy. Extirpation of the duodenal bulb reduced the postprandial acid output to or below preantrectomy levels. The findings indicate that the antrobulbar region exerts a complex influence on gastric acid secretion which may result in stimulation or inhibition of the HCl glands. Removal of the pyloric antrum and the duodenal bulb does not effectively reduce postprandial acid secretion.
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PMID:Role of antrum and duodenum in the control of postprandial gastric acid secretion and plasma gastrin concentration in dogs. 117 87

Dogs were provided with mucosal septal pouches of the fundic stomach and of the duodenal bulb. Gastric secretion was stimulated by intravenous infusion of submaximal doses of porcine gastrin or the stable choline ester Urecholine. Acid perfusion of bulbar pouches profoundly inhibited acid responses to gastrin. Bulbar acidification produced little or no reduction in acid secretion induced by Urecholine. Small doses of Urecholine do not release gastrin in the dog but may induce acid secretion, mainly by direct cholinergic stimulation of the HCl glands. The fact that Urecholine-induced acid secretion was not inhibited in the present experiments is consistent with the hypothesis that the bulbar mechanism does not interfere with cholinergic stimulation acting on the parietal cells.
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PMID:Effect of bulbar acidification on gastric acid responses to urecholine in Pavlov pouch dogs. 118 34

The influence of cyclic AMP on gastrin release from the canine antrum was investigated by a direct in vivo method. After removal of spleen, gastric corpus, pancreas and intestine an antral pouch was consecutively perfused with dibutyryl cyclic AMP, papaverin and bethanechol-HCl using a branch of the left gastroepiploic artery. A relevant rise of gastrin in portal blood was only observed during perfusion of bethanechol chloride. Thus cyclic AMP does not release gastrin from the canine antrum.
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PMID:[Effects of cyclic AMP and urecholine on gastric secretion in the dog]. 120 41

Stomach lesions induced by indomethacin (20 mg.kg-1 i.p.) and ethanol (1 ml 95% intragastrically) were studied after a 24 hour fast in rats which had undergone sialoadenectomy. The size of the lesions was correlated with gastric HCl secretion, with gastric vascular permeability (determined from the Evans blue concentration in the stomach tissue after its i.v. administration) and with the serum gastrin level. These parameters were also studied in sialoadenectomized rats and in animals given epidermal growth factor (EGF) (50 lg.kg-1). It was found that sialoadenectomy significantly (p < 0.01) raised the incidence of stomach lesions after the administration of indomethacin and also after ethanol (p < 0.05). A significant increase in both basal and stimulated HCl secretion was found after sialoadenectomy. Both indomethacin and ethanol also increased gastric vascular permeability in rats not subjected to sialoadenectomy, but sialoadenectomy raised it significantly compared with the non-sialoadenectomized group. The serum gastrin levels fell after sialoadenectomy and the decrease was significant after the subsequent administration of indomethacin or ethanol. The administration of EGF to sialoadenectomized rats lowered the incidence of stomach lesions, inhibited HCl secretion and reduced vascular permeability. The lowered susceptibility of the gastric mucosa to the formation of lesions in sialoadenectomized rats given indomethacin or ethanol can be regarded as the outcome of the uptake of EGF.
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PMID:Effect of sialoadenectomy on stomach lesions induced by indomethacin and ethanol in relation to gastric vascular permeability, the gastrin level and HCl secretion in rats. 128 10


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