Pentagastrin-induced Gastric Secretion Research Articles

Selective pharmacological blockade of parasympathetic and enteric ganglia

The blocking effects of two newly synthetized compounds, diisopropyldecylammonium iodide (IEM-1194) and 2,2,6,6-tetramethyldecylpiperidinium chloride (IEM-1559), on insulin- and pentagastrin-induced gastric secretion in chronic dogs, on stress-induced changes in gastric mucosa in rats, on vagus-induced effects in heart and intestine, on arterial blood pressure and on synaptic transmission through isolated ciliary and superior cervical ganglia in cats were studied. The effects observed were compared with those produced by hexamethonium (C 6), a conventional ganglionic blocking agent. Both IEM-1194 and IEM-1559 inhibited gastric secretion and acid output for a much longer time than C 6 did and effectively protected gastric mucosa against stress-induced erosions and hemorrhages. IEM-1194 blocked the vagus-induced decrease in heart rate and increase in duodenal motility for a longer time than did C 6 and also, in contrast to C 6, did not reduce the arterial blood pressure. The blockade of synaptic transmission through isolated ciliary and superior cervical ganglia produced by IEM-1194 and IEM-1559 was characterized by lower EC 50 and was more prolonged than that produced by C 6. In addition, both IEM-1194 and IEM-1559 were more potent blocking agents in ciliary ganglion than in superior cervical ganglion. It is suggested that IEM-1194 and IEM-1559 are selective blocking agents for parasympathetic and enteric ganglia versus sympathetic ganglia.

Dynamics of gastric acid inhibition by ranitidine in duodenal ulcer patients.

The dynamics of the inhibitory effect of ranitidine, a new H2-receptor antagonist, on histamine and pentagastrin-induced gastric secretion have been examined in duodenal ulcer patients. The inhibition by ranitidine of histamine-induced secretion was found to be competitive, whereas that of pentagastrin-induced secretion not competitive. Ranitidine was an effective inhibitor of pentagastrin-induced secretion for 8-12 h after administration. The availability of ranitidine, a powerful and long-acting inhibitor of gastric secretion, provides an opportunity of an alternative treatment from cimetidine for peptic ulcer and related diseases.

Role of adrenergic agonists on gastric secretion in the rat.

Following previous demonstration that isoproterenol stimulated and norepinephrine inhibited gastric acid secretion induced by secretagogues, role of adrenergic agonists was studied by measuring acidity the peptic activity of the effluent of the perfused rat stomach. Response of gastric secretion to isoproterenol was increased by theophylline treatment but was not affected by metiamide treatment. N6, O2'-Dibutyryladenosine 3', 5'-cyclic monophosphoric acid sodium salt monohydride (dibutyryl-c-AMP) stimulated gastric secretion in a dose-dependent manner. These results suggest the possibility that the action of isoproterenol in gastric acid secretion is mediated by c-AMP. However, gastric secretion induced by pentagastrin, histamine, or carbamylcholine was not affected by theophylline treatment. N2, O2'-Dibutyrylguanosine 3', 5'-cyclic monophosphoric acid sodium salt (dibutyryl-c-GMP) did not exert any effect on gastric secretion. Depression of pentagastrin-induced gastric secretion by norepinephrine was reversed by EGTA infusion. Moreover, Ca2+, depressed pentagastrin-induced gastric secretion. These results suggest that the action of norepinephrine is closely related to the concentration of Ca2+.

THE ROLE OF β1 ‐ AND β2‐ADRENOCEPTORS IN THE INHIBITION OF GASTRIC ACID SECRETION IN THE DOG

1. Characterization of the beta-adrenoceptors mediating inhibition of gastric acid secretion in the conscious Heidenhain pouch dog has been investigated by determination of the effects of propranolol, (+)-propranolol, practolol and H35/25 on salbutamol and isoprenaline-induced inhibition of gastric acid secretion. 2. The gastric antisecretory effect of salbutamol was significantly blocked by propranolol and H35/25 but not by practolol or (+)-propranolol. The effect of isoprenaline was significantly blocked by propranolol and practolol but not by H35/25 or (+)-propranolol. 3. It is concluded that both beta1- and beta2-adrenoceptors can mediate inhibition of pentagastrin-induced gastric secretion in conscious dogs with a Heidenhain pouch. Salbutamol exerts its antisecretory effect through beta2-adrenoceptors, whereas isoprenaline mediates its effects primarily through beta1-adrenoceptors. 4. The results are discussed with regard to the sub-classification of beta-adrenoceptors and to the possible role of adrenoceptors in the physiological control of gastric secretion. 5. In this study it is concluded that the tachycardia induced by isoprenaline or salbutamol is mediated primarily through reflexes activated by beta2-adrenoceptor mediated vasodilatation.

Effect of Somatostatin on Pentagastrin Stimulated Secretion by Isolated Canine Stomachs, Perfused <i>ex vivo</i> with Homologous Blood

The effect of somatostatin on pentagastrin-induced gastric secretion was assessed on 6 isolated canine stomachs perfused ex vivo with homologous blood. Hormones were given at a constant rate into the gastric arterial circulation. Somatostatin caused inhibition of the HCl concentration and output and reduced the secretion volume in all stomachs studied. The output but not the concentration of pepsin was also reduced.

The effect of calcium and calcitonin on pentagastrin-induced gastric secretion in intact and thyroidectomized dogs

The effect of calcium and calcitonin on pentagastrin-induced gastric secretion in intact and thyroidectomized dogs

Effect of Growth Hormone Release-Inhibiting Hormone on Gastric Secretion, Mucosal Blood Flow, and Serum Gastrin

In dogs with gastric fistulae and Heidenhain pouches (HP) growth hormone release-inhibiting hormone (GH-RIH) infused intravenously in a dose of 2.5 mug per kg per hr inhibited almost completely acid and pepsin responses to pentagastrin, Urecholine, and a peptone. Histamine-induced acid secretion was more resistant to the inhibition by GH-RIH, and only acid secretion evoked by the lower doses of histamine was suppressed by this peptide. The inhibition of pentagastrin-induced gastric secretion was associated with a marked reduction in mucosal blood flow. The ratio of aminopyrine concentration in the gastric juice and blood plasma was not significantly changed by GH-RIH, indicating that the reduction in mucosal blood flow was secondary to an inhibition of gastric secretion. Gastric acid and serum gastrin responses to a peptone meal adjusted to pH 5.0 and kept in the main stomach at this same pH by intragastric titration were significantly decreased by GH-RIH, indicating that the observed acid inhibition could be attributed at least in part to the suppression of gastrin release. GH-RIH inhibited acid secretion from HP stimulated by liver extract in HP. The finding that GH-RIH inhibits gastric secretion induced by exogenous stimulants as well as by the direct chemical stimulation of the HP mucosa without changing serum gastrin level suggests that the major action of GH-RIH is a direct suppression of the oxyntic glands.

Implication of gastric mucosal histamine in inhibition by isoprenaline of pentagastrin-induced gastric secretion.

1 The effect of isoprenaline on pentagastrin-induced gastric secretion was studied in conscious rats with Heidenhain pouches. The influence of isoprenaline on pentagastrin-induced release and formation of gastric mucosal histamine was also examined.2 Isoprenaline strongly inhibited pentagastrin-induced acid secretion, an inhibition which could not be overcome by increasing the dose of pentagastrin.3 Propranolol blocked the inhibitory effect of isoprenaline on pentagastrin-induced acid secretion.4 Isoprenaline enhanced pepsin secretion induced by pentagastrin, an effect which was blocked by propranolol.5 Isoprenaline reduced the increase in formation and release of gastric mucosal histamine following pentagastrin infusion, an inhibitory influence which was almost completely blocked by propranolol.6 The inhibition by isoprenaline of pentagastrin-induced acid secretion is tentatively related to alterations in gastric mucosal histamine occurring simultaneously.

The Effect of Glucagon on Pentagastrin-Induced Gastric Secretion of Sodium, Potassium, and Calcium in Man

Christiansen, J. & Hendel, L. The effect of glucagon on pentagastrin-induced gastric secretion of sodium, potassium, and calcium in man. Scand. J. Gastroent. 1974, 9, 437–440.The effect of glucagon on gastric secretion of Na, K, and Ca was studied in 7 healthy individuals. Glucagon (20 µg/kg-hr) was administered as a continuous intravenous infusion on a background infusion of pentagastrin (1 µg/ kg-hr). Sodium output was reduced, but the ratio Na concentration/secretory rate increased, indicating a relative increase in sodium output. Potassium secretion was significantly inhibited. Calcium concentration increased slightly, and output was inhibited to the same degree as volume secretion.

The effect of aminophylline on pentagastrin-induced gastric secretion in the dog.

The effect of aminophylline on gastric hydrochloric acid secretion was investigated in five dogs each with a Heidenhain pouch (HP) and gastric fistula (GF). Aminophylline administered intravenously in a single dose of 20 mg/kg during the resting state had no effect on gastric secretion. However, when this methylxanthine was administered during the secretory response to pentagastrin, it augmented the action of this peptide. On the basis of indirect evidence, it may be suggested that both agents act by increasing the cyclic adenosine monophosphate level in the gastric mucosa.

Mechanism of the inhibitory action of endogenous cholecystokinin and caerulein on pentagastrin--induced gastric secretion.

In dogs with vagally innervated gastric pouches (PP), gastric fistulas, and pancreatic fistulas, half maximal response to pentagastrin has been obtained. Caerulein given intravenously in doses ranging from 60 to 500 ng/kg-hr caused a dose-related inhibition of PP response to pentagastrin with the maximum of about 72% reached at the dose of 250 ng/kg-hr caerulein. Endogenous cholecystokinin (CCK) released by intraduodenal instillation of L-leucine and L-tryptophan mixture reduced acid response from PP by about 50% and caused an increase in pancreatic protein output equal to that reached with 120 ng/kg-hr of caerulein. Following surgical conversion of PP to Heidenhain pouch (HP), endogenous CCK and doses of caerulein producing an equal rate of pancreatic protein secretion were ineffective in the inhibition of pentagastrin-induced gastric acid secretion from HP. Stimulation by pentagastrin combined with a threshold dose of Urecholine increased the susceptibility of HP to inhibition by caerulein. From these r...

Pentagastrin-induced gastric secretion in dogs. Modulation by drugs acting on the tone of the autonomic nervous system.

Pentagastrin (0.2–6.4 μg/kg s.c.) given to conscious dogs supplied with a gastric fistula, caused a log dose-dependent gastric secretion of volume, H+, Na+, K+, Ca

Action of serotonin on gastric (proventriculus) secretion in chickens

1. 1. Serotonin and duodenal distension inhibited basal, histamine-induced, and pentagastrin-induced gastric secretion in chickens. 2. 2. In UML- 491 and reserpine pre-treated chickens, the inhibitory effects of duodenal distension and serotonin on gastric secretion were abolished. 3. 3. In UML- 491 pre-treated chickens serotonin did not inhibit the histamine- and pentagastrin-stimulated gastric secretion. 4. 4. There is no species difference in the action of serotonin on gastric secretion.

Effect of caerulein on histamine and pentagastrin-induced gastric secretion in man.

In 6 human subjects caerulein, a decapeptide isolated from frog skins, slightly stimulated gastric acid secretion when given alone. This peptide, added in a dose of 0.1µg/kg/hr to intravenous infusion of pentagastrin in a dose of 2.0µg/kg/hr, produced about 50% inhibition of near maximal gastric acid secretion. In 8 human subjects, however, it evidently increased gastric acid response to histamine diphosphate infused intravenously in a dose of 40 µg/kg/hr. The hypothesis of hormonal interaction was applied to explain the inhibitory and stimulatory effect of caerulein on pentagastrin and histamine-induced gastric acid secretion in man.

Role of the thyroid gland during glucagon-induced hypocalcemia in the dog.

ARTICLESRole of the thyroid gland during glucagon-induced hypocalcemia in the dogLV Avioli, SJ Birge, S Scott, and W ShieberLV Avioli, SJ Birge, S Scott, and W ShieberPublished Online:01 Apr 1969https://doi.org/10.1152/ajplegacy.1969.216.4.939MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByThe early prognostic value of inflammatory markers in patients with acute pancreatitisClinics and Research in Hepatology and Gastroenterology, Vol. 43, No. 3Prevention of hypercalcaemic nephropathy and tissue calcification by glucagon during phosphate infusionMedical Hypotheses, Vol. 53, No. 1Acute Pancreatitis: DiagnosisControl of Calcium Regulating Hormones in the Vertebrates: Parathyroid Hormone, Calcitonin, Prolactin, and StanniocalcinIntraperitoneal free fatty acids induce severe hypocalcemia in rats: A model for the hypocalcemia of pancreatitis3 December 2009 | Journal of Bone and Mineral Research, Vol. 5, No. 12Calcitonins — Physiological and Pharmacological AspectsHypocalcemia Associated with Calcium-Soap Formation in a Patient with a Pancreatic FistulaNew England Journal of Medicine, Vol. 315, No. 8Calcitonin as an Anorectic AgentGlucagon and Liver RegenerationGlucagon in Human Endocrine and Exocrine DisordersInfluence of Glucagon on Water and Electrolyte MetabolismSerum calcium and inorganic phosphorus level ofRana tigrina in response to glucagon administrationExperientia, Vol. 39, No. 1Effect of glucagon on magnesium renal reabsorption in the ratPfl�gers Archiv European Journal of Physiology, Vol. 392, No. 4Calcitonin SecretionHormonal Modifiers of Mineral Metabolism Other Than Parathyroid Hormone, Vitamin D, and CalcitoninChemistry of the Gastrointestinal Hormones and Hormone-like Peptides and a Sketch of Their Physiology and PharmacologyEffect of glucagon administration on serum calcium and inorganic phosphorus in the freshwater mud eel,Amphipnous cuchiaExperientia, Vol. 37, No. 10The role of calcitonin in hypocalcemia in acute experimental pancreatitisExperientia, Vol. 37, No. 5Calcitonin reduces feeding in man, monkey and ratPharmacology Biochemistry and Behavior, Vol. 12, No. 4Response of calcitonin cells, parathyroid, and serum electrolytes during glucagon-induced hypocalcemia in the mongoose, Herpestes edwardsi (Geoffroy)General and Comparative Endocrinology, Vol. 37, No. 4The Relationship Between Glucagon and Hypocalcaemia in Infants of Diabetic MothersEcological Factors in Learning Disabilities18 August 2016 | Journal of Learning Disabilities, Vol. 11, No. 8The first 24 hours of acute pancreatitisThe American Journal of Medicine, Vol. 64, No. 5ParathyreoideaCytophysiology of Thyroid Parafollicular CellsGlucagon, Insulin and their Hepatic Receptors: An Endocrine Pattern Characterizing Hepatoproliferative Transitions in the RatCONTROL OF ANIMAL CELL PROLIFERATIONSerum Calcitonin in Acute Pancreatitis in Man29 October 2018 | Scandinavian Journal of Gastroenterology, Vol. 12, No. 1Parathormone Levels vs. Parathormone FunctionNew England Journal of Medicine, Vol. 294, No. 10Pancreatitis and hyperparathyroidismPostgraduate Medical Journal, Vol. 52, No. 604CalcitoninPathophysiology of the Exocrine PancreasHaemorrhagic and necrotizing pancreatitisBritish Journal of Surgery, Vol. 62, No. 3Glucagonoma and A-Cell HyperplasiaClinics in Gastroenterology, Vol. 3, No. 3The Effect of Glucagon on Pentagastrin-Induced Gastric Secretion of Sodium, Potassium, and Calcium in Man16 October 2020 | Scandinavian Journal of Gastroenterology, Vol. 9, No. 5EARLY NEONATAL HYPOCALCÆMIAThe Lancet, Vol. 303, No. 7865LITHIUM AND HALOPERIDOL IN MOVEMENT DISORDERSThe Lancet, Vol. 303, No. 7865The ParathyroidsCalcium metabolism in pancreatic diseaseThe American Journal of Clinical Nutrition, Vol. 26, No. 3BIBLIOGRAPHYPancreatic Islet Cells in Experimental Hypo- and Hyperparathyroidism in Rats2 March 2011 | Upsala Journal of Medical Sciences, Vol. 77, No. 3Hypocalcemia in infants of diabetic mothersThe Journal of Pediatrics, Vol. 81, No. 3Glucagonoma as part of the polyglandular adenoma syndromeThe American Journal of Medicine, Vol. 52, No. 5Fragen der Calcitonin-ForschungKlinische Wochenschrift, Vol. 50, No. 1Control of secretion of parathyroid hormone and calcitonin in mammals and birdsGeneral and Comparative Endocrinology, Vol. 3Gastrointestinal Effects of Calcitonin in ManSerum Calcium and Gastric Secretion in Chronic Gastric Fistula Rat: Influences of Parathyroid Hormone and CalcitoninEuropean Journal of Clinical Investigation, Vol. 1, No. 6EVIDENCE FOR A ROLE OF CYCLIC AMP IN THE RELEASE OF CALCITONIN*16 December 2006 | Annals of the New York Academy of Sciences, Vol. 185, No. 1Langzeitwirkung von Glucagon auf die MagensekretionKlinische Wochenschrift, Vol. 49, No. 22Thyrocalcitonin and its role in calcium regulation in mammalsJournal of Experimental Zoology, Vol. 178, No. 1Acute PancreatitisGastroenterology, Vol. 61, No. 3Physiologie und Biochemie der endokrinen Regulationen und KorrelationenREFERENCESWhy hypocalcemia in pancreatitis?The American Journal of Surgery, Vol. 120, No. 6Glucagon in Medicine: New Ideas For an Old HormoneMedical Clinics of North America, Vol. 54, No. 1Multiple endocrine adenomatosisThe American Journal of Medicine, Vol. 47, No. 4 More from this issue > Volume 216Issue 4April 1969Pages 939-945 Copyright & PermissionsCopyright © 1969 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1969.216.4.939PubMed5775891History Published online 1 April 1969 Published in print 1 April 1969 Metrics

Effect of orally administered prostaglandin E1 on gastric secretion and gastrointestinal motility in man.

The effects of prostaglandin E1 administered orally in doses of 10-40 mug/kg were studied in 3 healthy male subjects aged 30 31 and 38 years to determine whether the prostaglandin inhibited the secretion of gastric juices. There was no inhibition of pentagastrin-induced gastric secretion. After higher doses of prostaglandin were administered gastric juice contained large amounts of bile. Prostaglandin E1 administration also increased intestinal motility resulting in loose feces. The findings show that prostaglandin E1 administered orally in humans fails to inhibit gastric secretion in doses which have effects on gastrointestinal motility.