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 effects of metiamide, a histamine H2-receptor antagonist, and propranolol, a beta-adrenergic blocking agent, on gastric secretion were studied in anesthetized dogs. Metiamide, 1.45 mg/kg i.v., markedly inhibited the gastric secretion induced by a continuous i.v. infusion of tetragastrin (8 microng/kg-hr), histamine dihydrochloride (160 microng/kg-hr), or methacholine bromide (100 microng/kg-hr). Propranolol 0.5 or 1.0 mg/kg i.v. produced a significant potentiation of tetragastrin-induced gastric secretion but no influence of the secretion induced by methacholine. Propranolol at 5 or 10 mg/kg i.v. produced a slight reduction of the tetragastrin-induced secretion and a significant reduction of methacholine-induced secretion. Histamine-induced gastric secretion was not affected by propranolol at either 1 and 10 mg/kg i.v. These findings lend support to the hypothesis that interactions among histamine, gastrin and acetylcholine receptors do occur though the degree would not be the same in all directions.
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PMID:Effects of metiamide and propranolol on gastric secretion in anesthetized dogs. 1 25

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

To study the beta-adrenergic contribution to the hypoglycaemic stimulation of gastric acid and gastrin release the effect of an equal and extensive beta-adrenergic blockade with three drugs was studied. Propranolol was investigated in 12, pindolol in 22, and practolol in 11 patients. Fasting concentration of gastrin serum and spontaneous acid secretion were not reduced by the drugs. Propranolol eliminated the gastrin response to hypoglycaemia, pindolol reduced it, and practolol caused no alteration. The hypoglycaemic acid response was reduced by all three drugs, propranolol reduced the response to one-half and was the strongest inhibitor, practolol the weakest. It is concluded that beta-adrenergic receptors may be of major importance for the hypoglycaemic stimulation of the stomach, but the receptors respond differently from the receptors in the heart.
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PMID:On the beta-adrenergic contribution to the gastric acid and gastrin responses to hypoglycaemia in man. 106 46

The importance of beta-adrenergic receptor activity for ulcer formation was studied. In rats fasted for 48 hours, ulcers in the rumen were produced constantly after 17 hours of pyloric ligation. d,1,Propranolol in doses of 1 to 30 mg/kg given 4 times during 12 hours caused a dose-dependent inhibition of ulcer formation. The ulcero-protective potency of d,1,propranolol was about 20 times that of d,propranolol. No explanation of the ulcero-protective effect was observed when the gastric acid secretion was studied after 17 hours. Serum gastrin concentration after 17 hours of ligation was in all animals less than 5 pmol per liter, i.e. below one-third of the normal fasting value. For all pharmacological effects apart from beta-adrenergic blockage, d,1, and d,propranolol do not differ, while the results presented here suggest that intact beta-adrenergic receptor activity is important for the development of gastric ulcers in the pylorus-ligated rat. The mechanism behind the ulcero-protective effect of beta-adrenergic blockage remains to be solved.
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PMID:Beta-adrenergic mechanisms and ulcer formation in pylorus-ligated rats. 118 4

The effect of gastric distension on plasma cholecystokinin (CCK), pancreatic polypeptide (PP) and gastrin concentrations was investigated in healthy volunteers. Fundic and antral distension was achieved by balloons attached to a gastric tube and inflated with 300 and 600 ml and 100 and 200 ml of air for fundic and antral distension, respectively. Gastric juice was continuously aspirated. Fundic distension was additionally studied during a concomitant intravenous infusion of atropine (5 micrograms/kg/h) or a bolus injection of propranolol (2 mg). Fundic distension with 300 ml caused a significant increase in PP release (+17% above basal). Distension with 600 ml significantly stimulated CCK (+81%), gastrin (+31%) and PP output (+74%) over 30 min. Atropine completely blocked PP release and almost abolished CCK release, whereas gastrin output was enhanced. Propranolol did not prevent CCK release induced by fundic distension, whereas gastrin and PP responses were diminished. Antral distension did not cause any significant changes in hormone response. In conclusion, we demonstrated a gastric phase of CCK release which is atropine sensitive, but not influenced by propranolol.
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PMID:Cholecystokinin release by gastric distension--an atropine-sensitive mechanism. 228 97

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

To investigate the possible role of adrenergic nerves in neurally mediated gastrin release, we evaluated the effect of selective adrenergic blockade on the serum gastrin response to gastric distention in healthy human subjects. On separate days, 2 mg of propranolol (beta-adrenergic antagonist), 5 mg of phentolamine (alpha-adrenergic antagonist), or saline (control) was injected intravenously just before distending the stomach with 700 ml of isotonic saline. For 30 min following distention, intragastric pH was kept constant at 5.0 by in vivo titration. Propranolol reduced distention-induced gastrin release by approximately 90% (p less than 0.02), whereas phentolamine had no significant effect on the gastrin response to distention. In additional experiments, we evaluated the effect of the same doses of propranolol or phentolamine on the exaggerated gastrin response to gastric distention that occurred during cholinergic blockade with atropine. In the presence of atropine (2.3 microgram/kg i.v.), propranolol significantly (p less than 0.01) reduced distention-induced gastrin release, whereas phentolamine significantly enhanced the gastrin response to distention (p less than 0.01). We conclude that: (1) distention-induced gastrin release was reduced by propranolol, suggesting that gastric distention releases gastrin by a beta-adrenergic mechanism and (2) distention-induced gastrin release was enhanced by phentolamine, but only in the presence of atropine. Thus, adrenergic nerves appear to regulate the gastrin response to gastric distention in humans: beta-adrenergic pathways stimulate gastrin release, and alpha-adrenergic pathways may inhibit gastrin release under certain circumstances.
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PMID:Adrenergic regulation of distention-induced gastrin release in humans. 612 Aug 77

The effect of adrenergic agonists and antagonists on the secretion of gastric somatostatin-like immunoreactivity (SLI) and gastrin was investigated in an isolated, vascularly perfused rat stomach preparation. Two- to six-fold increases in SLI secretion induced by isoproterenol, epinephrine, and norepinephrine were completely abolished by propranolol but were not influenced by phentolamine. Propranolol did not alter glucagon- and DB-cAMP-induced stimulation of SLI release. Experiments in which the beta 2-agonist salbutamol and the beta 1- and beta 2-blockers practolol and H35/25 were used showed that both subtypes of beta receptors are involved. Gastrin secretion revealed only minor changes in dose-response studies with a wide range of isoproterenol concentrations (2 X 10(-8) to 1.5 X 10(-4) M). The results obtained in this study suggest that in rats 1) the SLI response to adrenergic agonism is predominantly mediated by beta receptors; 2) both beta 1- and beta 2-adrenergic receptors are involved; 3) under in vitro conditions, adrenergic agonism is a weak stimulus for gastrin secretion.
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PMID:Adrenergic control of rat gastric somatostatin and gastrin release. 614 72

Using a newly developed system for culturing canine fundic mucosal cells, we examined regulation of the secretion of somatostatinlike immunoreactivity (SLI) by cholinergic and adrenergic transmitters. Enzyme-dispersed canine fundic mucosa cells were enriched in SLI content by counterflow elutriation and cultured on collagen for 42 h. Epinephrine alone, and in combination with gastrin, stimulated SLI secretion in a dose-dependent fashion. Propranolol did not alter the response to dibutyryl cAMP or gastrin but produced a parallel, rightward shift of the epinephrine dose-response curve with the dissociation constant (Ki) determined to be 14 nM by nonlinear curve fitting. Phentolamine, an alpha-adrenergic antagonist, enhanced SLI secretion in response to epinephrine, an effect reversed by the alpha 1-agonist methoxamine but not by the alpha 2-agonist clonidine. However, neither methoxamine nor clonidine alone inhibited the response to the beta-selective adrenergic agonist isoproterenol; thus, the existence of an adrenergic alpha 1-inhibitory receptor remained uncertain. Carbachol noncompetitively inhibited SLI secretion stimulated by gastrin, epinephrine, and dibutyryl cAMP. Atropine produced a parallel rightward shift of the carbachol dose-response curve (Ki = 0.4 nM). Pirenzepine also inhibited the effects of carbachol (Ki = 35 nM). Our studies suggest that SLI-containing cells in the canine fundic mucosa possess stimulatory beta-adrenergic receptors and inhibitory muscarinic receptors.
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PMID:Autonomic regulation of somatostatin release: studies with primary cultures of canine fundic mucosal cells. 614 98

To study whether specific beta-adrenergic mechanisms contribute to the hypoglycaemic activation of gastrin and gastric acid secretion, the effects of racemic and dextroisomer propranolol (0.1 mg/kg, intravenously) were studied during insulin tests (0.2 IU/kg) in 13 persons. dl-Propranolol inhibited the gastrin response to hypoglycaemia markedly and more than the insignificant alteration observed after d-propranolol. Gastric acid response to hypoglycaemia was significantly reduced by dl-propranolol and not by d-propranolol. The findings demonstrate that non-beta-adrenergic effects of propranolol on the stomach are minor and that specific beta-adrenergic mechanisms are directly or indirectly involved in the hypoglycaemic stimulation of the stomach.
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PMID:Specific beta-adrenergic mechanisms in the hypoglycaemic activation of gastrin and gastric acid secretion. 637 65


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