Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The vascular bed of the submandibular gland in situ was perfused with blood through the glandular artery at a constant pressure in anesthetized dogs. All drugs were administered intra-arterially. 2. Vasoactive intestinal peptide (VIP), secretin and acetylcholine produced a dose-dependent increase in blood flow through the artery (vasodilatation) but glucagon was almost ineffective. 3. Dose-blood flow response curves for VIP and secretin were parallel, and VIP was about 100 times as potent as secretin on a molar basis. Dose-blood flow response curves for acetylcholine were flatter than those for VIP and secretin. Acetylcholine was approximately as potent as secretin on a molar basis. 4. No tachyphylaxis developed to the vasodilator action of VIP. 5. The vasodilator responses to VIP and to electrical stimulation of the chordolingual nerve were scarcely modified by (-)-hyoscyamine in doses that fully antagonized the vasodilator response to acetylcholine. 6. VIP, secretin and glucagon were ineffective in eliciting salivary secretion. 7. The possibility that VIP is released from parasympathetic vasodilator nerves and mediates the atropine-resistant vasodilatation in the dog submandibular gland is discussed.
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PMID:Assessment of the effects of vasoactive intestinal peptide (VIP) on blood flow through and salivation of the dog salivary gland in comparison with those of secretin, glucagon and acetylcholine. 43 91

The responses of plasma gastro-entero-pancreatic (GEP) hormones and free fatty acids (FFA) to a standard mixed meal before and after starvation have been measured. Raised insulin, glucose and FFA levels were found following refeeding after starvation and levels of secretin and C-terminal glucagon-like-immunoreactivity (C-GLI), raised by starvation, were rapidly suppressed on refeeding. The responses of gastrin and N-terminal glucagon-like-immunoreactivity (N-GLI) to a standard mixed meal were not altered by starvation. Although this study does not directly support that secretin and glucagon are responsible for the hyperglycaemia or hyperinsulinaemia of starvation diabetes, a role for both hormones in the raised FFA levels is proposed, as well as a role for glucagon in the initial hyperglycaemic response to a meal after starvation.
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PMID:The gastro-entero-pancreatic hormone secretion after a mixed meal in normal subjects before and after a 72 hour period of starvation. 44 30

Inhibition of secretin-stimulated pancreatic secretion by glucagon was studied in anesthetized dogs. Two external pancreatic fistulas were prepared in dogs for both simultaneous and separate collection of pancreatic juice secreted by the right and left lobes. Two series of experiments were preformed. In the first, graded doses of glucagon (2.5 to 20 micrograms/kg/hr) were administered against a background infusion of 2 CHR U/kg/hr of secretin. In the second, a constant dose of glucagon (20 micrograms/kg/hr) was given against a background infusion of secretin doubling from 1 to 8 U/kg/hr. Infusion of glucagon was started when flow rate became nearly constant, and continued for 60 minutes in each dose. Glucagon produced the dose-related reduction in flow rate and bicarbonate secretion, but not in amylase secretion. This inhibitory effect was almost the same in size between the right and left lobes. No significant change of plasma secretin was observed during glucagon infusion. Michealis-Menten analysis of the dose in slopes (Km) and similar intercepts of Y-axis (CMR). These results suggest that glucagon inhibits competitively secretin-stimulated pancreatic secretion by acting probably on the same receptor as secretin.
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PMID:Interaction of secretin and glucagon on exocrine pancreatic secretion. 44 88

Smooth muscle adenylate cyclase of a membrane preparation of canine gastric antrum has been characterized, and the effect of hormonal and neuronal agents examined. The enzyme is active in the presence of Mg2+ or Mn2+, but is inhibited by Ca2+. The Km is 0.5 mM ATP, similar to the Km of skeletal muscle adenylate cyclase. The enzyme is activated by isoproterenol but not norepinephrine, consistent with a beta 2-catecholamine receptor-adenylate cyclase interaction. Secretin activates the enzyme in concentrations as low as 1 . 10(-11) M, while glucagon was effective only at 1 . 10(-6) M. Prostaglandin E1 and E2 have a biphasic effect with activation of adenylate cyclase at 1 . 10(-5) M and a small but significant inhibition of enzyme activity at 1 . 10(-11) M.
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PMID:Effect of hormonal and neuronal agents on adenylate cyclase from smooth muscle of the gastric antrum. 45 75

The peptides usually called gastrointestinal hormones belong to a broader group of regulatory substances distributed in many parts of the body and delivered to their targets not only by the blood but also by neural and paracrine paths. The neural, endocrine, and paracrine cells as a group might be called "regulator cells" and the chemical messengers they produce might be called "regulins." Twenty peptides have been isolated from the alimentary tract and pancreas: 12 have been sequenced, 4 have been partially sequenced, and 4 more have been identified only by immunoreactivity. Gastrin, gastric inhibitory peptide, glucagon, insulin, and secretin can be regarded as established hormones that are released into the blood by identified stimuli and produce identified physiological responses. The evidence for the hormonal status of cholecystokinin, pancreatic polypeptide, and motilin is incomplete but suggestive. The possible physiological roles of the other 12 peptides remain to be determined. If specific antagonists of these peptides can be found, they will greatly assist in elucidating the peptides' physiological roles.
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PMID:Chemical messengers: a view from the gut. 45 21

Strong secretin-like immunofluorescence has been demonstrated in endocrine-like cells from the gastric epithelium of Styela. These cells also stain with lead haematoxylin and exhibit a brilliant formaldehyde-induced fluorescence, but do not show any other cytochemical features characteristics of the mammalian APUD series. Tests with antisera to glucagon, gastrin and somatostatin all proved negative. In the oesophagus tests with all four antisera proved negative. The significance of these results is discussed in relation to the phylogeny of vertebrate gastro-intestinal hormones.
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PMID:A cytochemical and immunofluorescence study of endocrine cells in the gut of the ascidian Styela clava. 46 92

When isolated rat liver cells were incubated in the presence of vasoactive intestinal peptide at the concentrations ranging from 0.2 microgram to 2 micrograms per ml, glycogenolysis was maximally stimulated within 15 min. However, somatostatin inhibited the liver glycogenolysis. The combined addition to the incubation medium showed that insulin and somatostatin inhibited the stimulated glycogenolysis induced by vasoactive intestinal peptide, while vasoactive intestinal peptide plus secretin showed no additive effect on glycogenolysis, as compared with single the addition of vasoactive intestinal peptide. On the other hand, the additon of glucagon to vasoactive intestinal peptide showed additive effects on glycogenolysis. These results suggest that the receptor site for vasoactive intestinal peptide may be distinguishable from that for glucagon. Extracellular calcium ions were demonstrated to play an important role in the modulation of vasoactive intestinal peptide-induced glycogenolysis. The evidence presented in this paper indicates that glucose metabolism may be partly regulated by the direct action of vasoactive intestinal peptide on hepatocytes, which is referred to as an enterohepatic axis and that the axis is inhibited by insulin and somatostatin.
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PMID:Effects of vasoactive intestinal peptide on glycogenolysis in cultured liver cells. 47 14

The inhibitory effects of intravenous infusions of secretin, glucagon and caerulein on the gastric acid response to bombesin were studied in 8 duodenal ulcer patients. Bombesin was found to be a very potent stimulator of gastric acid secretion in patients with duodenal ulcer. There were no significant differences in acid outputs per 15-min period between bombesin infused in a dose of 0.9 microgram/kg/h and pentagastrin infusion administered in a maximal dose, at a rate of 6.0 microgram/kg/h. Secretin (1 U/kg/h), glucagon (30 microgram/kg/h) and caerulein (0.1 microgram/kg/h) produced significant decreases in gastric acid secretion evoked by bombesin given in a dose of 0.9 microgram/kg/h. Percentages of inhibition were 48.6, 45.2 and 35.5, respectively. It is supposed that secretin and glucagon given in pharmacological doses are capable of interfering with the action of gastrin released from antrum by means of bombesin on the parietal cell by noncompetitive kinetics. Caerulein administered in a pharmacological dosis, however, can inhibit the effect of gastrin released by bombesin on the parietal cells by a competitive kinetic.
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PMID:Inhibition of bombesin-stimulated gastric acid secretion by secretin, glucagon and caerulein in patients with duodenal ulcer. 48 52

Because the gastrointestinal hormones are known to dilate the splanchnic vasculature, their effects on transport of water and solutes during peritoneal dialysis were studied in an experimental model, the rabbit. In unanesthetized rabbits, dialysate volume was calculated by isotope dilution, and clearances were estimated by dialysate/plasma concentration ratio factored by minute volume. With isotonic dialysis solution, the mean increment in dialysate volume per minute of intraperitoneal dwell was 0.19 ml/kg/min, and mean clearances of creatinine and urea were 0.71 and 0.90 ml/kg/min, respectively. When administered intravenously, secretin significantly augmented osmotically induced water flux, but not when given intraperitoneally. Neither glucagon nor cholecystokinin affected dialysate volume. Intravenously, but not intraperitoneally, glucagon increased peritoneal clearances of creatinine and urea to more than 150% of control values. Neither cholecystokinin nor secretin augmented significantly peritoneal mass transport when given by either route. The data suggest that the site of acton is the endothelial surface of the membrane, that the mechanisms of augmenting transport involve increased permeability and/or surface area, and that agents which combine an increase in mass transport and capillary filtration coefficient may be clinically useful.
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PMID:Effects of gastrointestinal hormones on transport by peritoneal dialysis. 51 2

The major restrictions to the transport of solute and solvent across the peritoneum are the limited peritoneal blood flow, area and permeability. Recent investigations have demonstrated that several vasoactive drugs influence transport parameters. Isoproterenol, nitroprusside, dipyridamole and dopamine exemplify drugs that dilate the splanchnic vasculature, thereby augmenting transport, whereas vasoconstriction induced by l-norepinephrine decreases clearances. The tissue prostaglandins affect peritoneal mass transport in accord with their known vasoactive effects, suggesting a role in modulating peritoneal blood flow. The gastrointestinal hormones vasodilate the splanchnic circulation. Exposure of the endothelial surface to glucagon markedly increases peritoneal mass transport, while secretin increases the ultrafiltration rate significantly. These preliminary studies suggest the possible future clinical use of drugs and hormones to augment the efficiency of peritoneal dialysis.
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PMID:Acceleration of peritoneal mass transport by drugs and hormones. 53 10


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