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Query: UNIPROT:P01350 (gastrin)
 9,683 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An in vitro technique that allows study of gastrin secretion from isolated pieces of rat gastric antrum was used to study the effect on gastrin release of agents known to increase intracellular cAMP levels. Isuprel (10(-5)M), PGE1 (10(-5)M), theophylline (10(-4)M), and dibutyryl cAMP (5 X 10(-4)M) did not affect gastrin release when used alone, but each enhanced arginine-stimulated gastrin release. A biphasic pattern of gastrin release in response to arginine was seen in all experiments. The studies emphasize the close functional similarity between the antral G cells and the B cells of the pancreatic islet.
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PMID:The effect on gastrin secretion of agents which increase the intracellular concentration of 3',5'-adenosine monophosphate. 17 Nov 47

Isoproterenol if given during methacholine stimulation in dogs neither depresses gastric secretion nor elevates serum gastrin. Therefore, we conclude that beta adrenergics (isoproterenol) are unlikely to be direct liberators of gastrin, but raise serum gastrin indirectly only if they inhibit gastric secretion.
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PMID:Do beta adrenergic agents directly stimulate gastrin secretion? 65 37

Isoproterenol infusions depress pentagastrin (PG)-stimulated secretion of acid and pepsin from both gastric fistulae and denervated (Heidenhain) pouches in conscious dogs. It was not found to do so if methacholine replaced gastrin. Propranolol reversed the isoproterenol depression of PG stimulation but had no effect on isoproterenol plus methacholine except on the fistula where both acid and pepsin were depressed. It is felt that PG and methacholine act by differing mechanisms both on chief and parietal cells.
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PMID:Adrenergic activity and gastric secretion. 77 88

1 The effect of isoprenaline on gastric secretion evoked by various means has been studied in conscious rats provided with Pavlov and Heidenhain pouches. 2 Interdigestive acid secretion in the Pavlov pouch was reduced by isoprenaline, whereas pepsin secretion was unaltered. 3 Central vagal stimulation effected by 2-deoxy-D-glucose injection evoked a gastric secretory response that was substantially reduced by isoprenaline. 4 2-Deoxy-D-glucose increased the mobilization of gastric mucosal histamine, an effect that was prevented by isoprenaline. 5 Isoprenaline infusion alone induced a slight increase in histamine mobilization and also a considerable elevation of immunoreactive serum gastrin concentration. 6 The secretory response to food in the Pavlov pouch was almost abolished by isoprenaline. 7 Although the acid response to histamine in the Heidenhain pouch was susceptible to isoprenaline inhibition, that to methacholine was not. 8 Pepsin secretion in the Heidenhain pouch preparation stimulated by histamine or methacholine seemed to be enhanced by isoprenaline.
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PMID:Further studies on the mode of action of isoprenaline on gastric secretion in the conscious rat. 97 74

Intravenous infusion of isoproterenol, a beta-adrenergic receptor stimulatory agent, increased serum gastrin concentration significantly more in patients with a duodenal ulcer than in healthy subjects. The rise in pulse rate, blood glucose concentration and in serum insulin was the same in both groups of subjects. Gastrin secretion was also increased significantly more in the patients than in the control subjects after a beef-meal. Basal serum gastrin concentrations were higher in the patients than in the control subjects and correlated to the rise in serum gastrin during both tests in the patients with a duodenal ulcer. Isoproterenol and meal stimulated gastrin secretion, expressed as percent of the basal value, were twice as higher in the patients as in the control subjects. The combined administration of isoproterenol and the meal had an additive effect on the rise in serum gastrin. Isoproterenol stimulated gastrin secretion was completely suppressed by propranolol, a beta-adrenergic receptor blocking agent, which had no effect on meal stimulated gastrin secretion. It is concluded that the mechanism of the hypersecretion of gastrin in patients with a duodenal ulcer did not involve a specific abnormality of the beta-adrenergic receptor or the receptor which recognized proteins and their digested products. There is no established role of beta-adrenergic receptor activity in the hypersecretion of gastrin in patients with duodenal ulcers. It is suggested that the beta-adrenergic receptor may have some yet unknown function unrelated to the acute secretory response of gastrin.
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PMID:The role of the beta-adrnergic receptor in the secretion of gastrin: studies in normal subjects and in patients with duodenal ulcers. 97 1

1. Gastric acid and mucosal blood flow responses to sustained gastrin stimulation were studied in anaesthetized cats. 2. Acid and mucosal blood flow showed identical rates of tachyphylaxis to both large (maximal) and small doses of gastrin. 3. Isopropylnoradrenaline infused either intravenously or close arterially to the stomach produced increases in blood flow unrelated to time following the peak response to large doses of gastrin, whereas increases in acid secretion appeared to be a part removal of the acid tachyphylaxis. 4. During stimulation by small doses of gastrin, isopropylnoradrenaline increased both blood flow and acid secretion above the peak responses to gastrin alone. 5. Increases in gastrin stimulated acid and mucosal blood flow were also produced by expansion of the blood volume by dextran-saline infusions. 6. The physiological significance of these findings is discussed. 7. It is concluded that tachyphylaxis of gastric acid secretion to gastrin may be a function of the primary tachyphylaxis of mucosal blood flow.
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PMID:Effects of isopropylnoradrenaline on tachyphylaxis of gastrin stimulated gastric acid secretion and mucosal blood flow in the anaesthetized cat. 124 24

Propranolol induces basal achlorhydria in 30.7% of the patients, decreases significantly the HCl secretion in 42.3%, does not change it in 25% and increases it in 1.9%. After histamine stimulation (Kay test) propranolol decreases HCl in 57% and increases it in 43% of the cases. Propranolol induces a significant decrease of carbon anhydrase in the gastric mucosa. Serum gastrin is not significantly decreased after propranolol treatment. Isoprenaline increases the HCl secretion in all the patients investigated. Propranolol suppresses the effect of isoprenaline in 28.6% of the cases, decreases it in 33%, does not change it in 19% and increases it in 19%. The action of isoprenaline is not influenced by atropine, so the mechanism of action of the beta agonist is non-cholinergic. The gastric juice volume is not changed significantly by the blockage or stimulation of beta receptors. The beta adrenergic nervous system stimulates HCl secretion.
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PMID:Beta adrenergic regulation of the hydrochloric acid secretion. 254 19

1. In conscious cats prepared with gastric fistulae gastric acid secretion in response to pentagastrin was found to reach a maximum after 45 min of stimulation, and to fade thereafter. Over the period 45-150 min of stimulation the fade was 5.4-7.8% of the maximum response per 15 min. 2. Once the response to pentagastrin had declined, acid secretion could not be restored by doubling the dose of pentagastrin, although an equisecretory dose of histamine could restore it. 3. Low doses of histamine were additive to the pentagastrin acid secretory response; they tended to prolong the peak response, but did not alter the subsequent fade of acid secretion. The histamine H1-receptor antagonist mepyramine did not affect maximal acid secretion or the fade of the pentagastrin response. 4. The beta-adrenoreceptor antagonist propranolol increased the secretory response to pentagastrin, whilst the alpha-adrenoreceptor antagonist phentolamine was without effect. Neither agent altered the fade of the pentagastrin response. Isoprenaline tended to inhibit pentagastrin-stimulated acid secretion and increase the rate of fade of the response. 5. The 5-hydroxytryptamine (5-HT) receptor antagonist methylsergide slightly enhanced the acid secretory response to pentagastrin, but did not alter the fade of the response. A low dose of 5-HT did not alter pentagastrin-stimulated acid secretion, whilst a higher dose of 5-HT inhibited it. 6. Tetra-, penta- and pentadecagastrin demonstrated tachyphylaxis, i.e. progressively reduced responses upon repeated stimulation, whilst histamine did not. A low dose of histamine did not prevent tachyphylaxis of the pentagastrin response. 7. It is concluded that fade of pentagastrin-stimulated acid secretion in the conscious cat cannot be satisfactorily explained by the failure of the acid secretory mechanism, depletion of histamine, release of 5-HT, or activation of histamine H1-, alpha- or beta-adreno-, or 5-HT-receptors. The similar characteristics of fade and tachyphylaxis of gastrin-stimulated acid secretion are consistent with a common gastrin receptor inactivation or desensitization mechanism.
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PMID:Investigation of mechanism of fade of gastrin-stimulated gastric acid secretion in the cat. 341 80

It has been hypothesized that secretin may act directly on gastrinoma through the adenylate cyclase system to cause stimulation of gastrin release. We studied gastrinoma cells in vitro to determine whether secretin would stimulate gastrin release directly and whether the gastrinoma cell membrane had a functional secretin receptor adenylate cyclase system. Fresh tumor was prepared in cell suspensions containing 1.5 X 10(6) viable cells and incubated for 2 hours with either 2 mM CaCl2 alone (control) or 2 mM CaCL2 and 0.025 U/ml secretin. The gastrin content of the cells in each incubation chamber and the medium were determined by radioimmunoassay and results were expressed as mean gastrin pg/microgram protein +/- SD. Under basal conditions the cellular gastrin content was 39.9 +/- 6.4 (control) compared with 16.7 +/- 2.1 (secretin). After 2 hours of incubation, cellular gastrin content increased in both groups: 68.5 +/- 11.9 (control) to 68.3 +/- 5.5 (secretin). However, the percent of gastrin released into the medium during incubation decreased by one half in both groups (control 37.3% +/- 4.0% to 22.2% +/- 3.0%; secretin 42.8% +/- 7.0% to 18.9% +/- 1.8%). Adenylate cyclase activity was assessed by measuring cAMP generation in fresh-frozen gastrinoma and cultured gastrinoma cell membranes. Isoproterenol (10(-5) M), PGE1 (10(-4) M), and GppNHp (guanine nucleotide) (10(-5) M) caused fivefold to 25-fold increases in cAMP generation. Secretin did not stimulate adenylate cyclase activity above basal (21.73 +/- 4.07 and 2.29 +/- 1.2 pmol cAMP/mg protein/min) for frozen and cultured gastrinoma, respectively. Secretin failed to stimulate gastrin release and adenylate cyclase in vitro. This suggests that secretin-stimulated gastrin release in vivo may not be due to a direct effect of secretin on the gastrinoma.
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PMID:Failure of secretin to stimulate gastrin release and adenylate cyclase activity in gastrinoma in vitro. 609 76

The interactions of adrenergic and cholinergic influences on the gastric D cell were studied using an isolated perfused rat stomach in vitro. The sevenfold increase in the release of somatostatin-like immunoreactivity (SLI) in response to isoproterenol (4 . 10(-8) M) was dose-dependently inhibited by acetylcholine (10(-5) to 10(-8) M) whereas gastrin levels increased in a dose-dependent manner. Both inhibition of stimulated SLI and augmentation of gastrin release were completely abolished by atropine (10(-6) M). Isoproterenol (8 . 10(-9) M)-induced stimulation of SLI secretion was not altered by atropine. Antral exclusion completely eliminated gastrin secretion but basal and beta-adrenergic stimulated SLI release was not influenced. It is concluded that (1) cholinergic agonism reverses the stimulatory action of adrenergic agonists on the D cell, and (2) SLI from the rat stomach in vitro originates almost exclusively in the fundic region.
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PMID:Adrenergic and cholinergic interactions in rat gastric somatostatin and gastrin release. 612 70


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