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

Dogs were provided with mucosal septal pouches of the stomach and of the duodenal bulb. In some dogs a drainage gastric cannula was inserted into the most dependent portion of the stomach. In dogs which were found to secrete acid spontaneously during a control period at the start of each experiment, the bulbar puches were perfused with 0.1 M HC1 for 5-120 min. Bulbar acidification rapidly and profoundly reduced the basal acid output. In dogs which did not secrete acid spontaneously during the control periodbulbar pouches were perfused with 0.1 M HC1 for 1 h. Bulbar acidification did not significantly influence the plasma gastrin concentration and no acid was secreted from the Pavlov pouches following such acidification. The present results support the hypothesis that reduction of the intrabulbar pH may contribute to the reduction of acid secretion during interdigestive periods. The physiological significance of of mechanisms in the upper intestine which induce acid secretion following a reduction of the intraluminal pH is questioned.
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PMID:Effect of bulbar acidification on basal secretion of acid and gastrin in dog. 0 71

The isolated, vagally innervated antral pouches in anesthetized dogs were irrigated with 095% acetylcholine chloride (Ach) or a 0.4 M mixture of non-essential amino acids (AA), or distended at 30 cm H2O pressure. In addition,2-deoxy-D-glucose (2-DG) was administered intravenously. Significant increases in antral venous gastrin, caused by gastrin releasers, were associated with a significant rise in cAMP content in the antral mucosa. Acidification of the antrum with simultaneous administration of 2-DG, and acidified AA abolished gastrin release, and significantly reduced mucosal cAMP. Acidified Ach and distension of the antrum with 0.1 N HC1 supressed gastrin levels without significantly changing the mucosal cAMP content. Since the augmented gastrin release was accompanied by an increased mucosal cAMP, the results suggest that cAMP participates in the action of gastrin secretagogues.
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PMID:Cyclic Amp and the release of antral gastrin. 19 27

Lower oesophageal sphincter response to infusion of graded doses (0.003--0.050 microgram kg-1min-1) of pentagastrin was evaluated in four antrectomised patients as well as in six healthy subjects and seven achalasic patients in whom inhibition of antral gastrin release was maintained by continuous acidification (HC1 0.1 N) and aspiration of gastric antrum. In normal subjects and in antrectomised patients doses of pentagastrin required for half-maximal gastric acid secretion (0.012 microgram kg-1min-1) produced statistically significant increases of LES pressure. In achalasic patients, the infusion of pentagastrin did not affect LES pressure. These data seem to indicate that gastrin plays, at least in some degree, a physiological role in the regulation of LES tone. Insensitivity of LES to pentagastrin in achalasia suggests that the raised sphincter pressure in this disorder can not be attributed to gastrin.
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PMID:Lower oesophageal sphincter response to intravenous infusions of pentagastrin in normal subjects, antrectomised and achalasic patients. 74 97

In ten normal subjects the effect of propranolol on serum gastrin concentration and HC1 secretion during insulin hypoglycemia (0.2 U/kg) was studied. Under the influence of propranolol (50 mug/kg intravenously in 3 min) the gastrin response to insulin was abolished. The insulin-induced HC1 secretion was reduced by propranolol from 38 to 18 mEq/2h (p less than 0.01). These results are compatible with the hypothesis of beta-adrenergic stimulation on serum gastrin concentration and HC1 secretion during insulin hypoglycemia.
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PMID:The influences of propranolol on serum gastrin concentration and hydrochloric acid secretion in response to hypoglycemia in normal subjects. 120 7

Basal and meat extract stimulated plasma gastrin (PG) levels and basal and stimulated gastric acid secretion were evaluated pre and postoperatively in duodenal ulcer patients who underwent parietal cell vagotomy without antral drainage (normal duodena) (PC, n=32) or selective vagotomy with drainage (pyloric stenosis) (SV +P, n=11). Before operation, both groups had comparable basal PG values of 52+/-13 pg/ml (PCVP) AND 51+/-18 PG/ML (SV+P), while the peak gastrin level to meat extract stimulation was 173+/-40 pg/ml for the total group of patients. After both operations basal PG levels increased (107+/-18 pg/ml (PCV) and 152+/-45 pg/ml (SV+P) and the gastrin response to meat extract stimulation was augmented after PCV, while the response after SV+P was the same as before operation. Patients with PCV often demonstrated an acid response following meat extract stimulation (3.6+/-0.9 mEq HC1/hr), and pentapeptide stimulation (18.8+/-2.0 mEq/hr) while patients with SV/P showed a minimal response (1.3+/-1.2 mEq HC1/hr meat extract), and 10.7+/-1.8 mEq/hr pentapeptide stimulation. The comparatively intact acid response in the PCV patients may augur a high ultimate recurrence rate.
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PMID:Basal and meat extract plasma gastrin before and after parietal cell vagotomy and selective gastric vagotomy with drainage in patients with duodenal ulcer. 124 15

Review of literature. Already low dosis of alcohol damage gastric mucosa; alcohol especially causes erosions. In spite of acute damage there is no proven correlation between alcohol and chronic gastritis. HC1 secretion is stimulated by low dosis of alcohol only; higher dosis have no effect on acid secretion. Nevertheless beer or wine stimulate acid secretion very intensively by gastrin liberation. -Low concentrations of alcohol have no influence on gastric emptying, but higher concentrations delay emptying, solid meals more than liquid meals.
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PMID:[Effect of alcohol on the stomach]. 267 57

The secondary structures of three gastrin analogs, HC1 X H-Trp-Nle-Asp(O-tBu)-Phe-NH2 (tetragastrin), pGlu-Ala-Tyr-Gly-Trp-Nle-Asp-Phe-NH2 (octagastrin), and H-Leu-(Glu)5-Ala-Tyr-Gly-Trp-Nle-Asp-Phe-NH2 (minigastrin) were studied by 1H-n.m.r. in dimethylsulfoxide and in trifluoroethanol. All three compounds were found to assume a random conformation in the former solvent, while some ordered secondary structure is present in trifluoroethanol even at the tetrapeptide level. This was shown by temperature studies and solvent titrations. At least four amide protons were found to be solvent shielded in the longer hormone.
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PMID:Conformational studies on gastrin related peptides by high resolution 1H-n.m.r. 369 83