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)

Species differences concerning the effects of alpha- and beta-receptor stimulation on glucagon release and carbohydrate metabolism have been reported. The aim of the present study was to investigate how the subtypes of alpha- and beta-receptors regulate the plasma levels of glucagon, insulin, glucose and free fatty acids in fasted rabbits. Epinephrine-induced 1) hyperglucagonaemia, 2) hypoinsulinaemia and 3) hyperglycaemia were significantly inhibited by alpha-2 receptor blockade (yohimbine), and not influenced by alpha-1 receptor blockade (prazosin). Isoproterenol-induced 1) hyperglucagonaemia was not affected by beta-1 or beta-2 receptor blockade, 2) hyperinsulinaemia was inhibited by a lower dose of beta-2 (ICI 118.551) than beta-1 receptor blockade (metoprolol), 3) hyperglycaemia was inhibited by beta-2 receptor blockade and 4) increases in the plasma levels of free fatty acids were blocked by beta-1 receptor blockade. It is concluded that in fasted rabbits: 1) plasma levels of glucagon are mainly increased by alpha-2 receptor stimulation, 2) plasma levels of insulin are decreased by alpha-2 receptor stimulation, and increased more by beta-2 than by beta-1 receptor stimulation, 3) plasma levels of glucose are increased by alpha-2 and beta-2 receptor stimulation and 4) the plasma levels of free fatty acids are increased by beta-1 receptor stimulation.
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PMID:Adrenergic effects on plasma levels of glucagon, insulin, glucose and free fatty acids in rabbits--influences of selective blocking drugs. 614 41

Fast-frozen pectoralis muscle samples were taken from normal chickens (lines 200 and 412) and chickens having hereditary muscular dystrophy (line 304). The glycogen phosphorylase activity ratio (activity without AMP/activity with AMP) was significantly greater in dystrophic muscles (0.306 +/- 0.046) than it was in normal muscles (0.090 +/- 0.023). Glucagon treatment did not cause any changes in phosphorylase activity ratios. Isoproterenol treatment of both normal and dystrophic muscles raised the phosphorylase activity ratio of normal muscles to 0.446 +/- 0.054, which was not significantly different from that of the dystrophic muscles. The dystrophic muscles had significantly less glycogen than normal muscles (23.3 +/- 2.8 compared with 36.8 +/- 2.8 mumoles glucosyl units/g of muscle). There was no relationship of muscular dystrophy to total phosphorylase activity (measured in the presence of 1 mM AMP) and to glycogen synthase activities measured without and with glucose 6-phosphate. Normal muscles had 28% less cAMP and 49% less cGMP than dystrophic muscles, but these differences were eliminated by treatment of the chickens with glucagon.
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PMID:Glycogen cycle enzymes and cyclic nucleotides in avian muscular dystrophy. 624 56

Male Wistar albino rats received three times daily for one to five days 0.25 to 5.0 mg/kg D,L-isoproterenol intraperitoneally. D.L-Isoproterenol injections provoked a time dependent- and dose-related cardiac hypertrophy. With moderate hypertrophy, a selective decrease in secretin-stimulated adenylate cyclase activity occurred. When heart hypertrophy was more pronounced, greater losses in secretin-, as well as in D,L-isoproterenol-, glucagon-, guanine nucleotide-, and fluoride-stimulated enzyme activity developed. Hormone stimulations of adenylate cyclase were more severely, curtailed (60 to 65%) than guanine nucleotide or fluoride stimulations (40 to 45%). The accompanying loss in beta-receptors (35%) was proportionately lower than the loss of D,L-isoproterenol sensitivity of adenylate cyclase. This complex pattern of adenylate cyclase desensitization in heart membranes from animals chronically treated with D,L-isoproterenol is reminiscent of that observed in heart membranes from spontaneously hypertensive rats.
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PMID:Early decrease in secretin-, glucagon-, and isoproterenol-stimulated cardiac adenylate cyclase activity in rats treated with isoproterenol. 628 Jul 26

Isoproterenol, dopamine, glucagon and dibutyryl cyclic AMP (DB-cAMP) increase renin release at low but not at control blood pressure. These findings suggest that autoregulated afferent arteriolar dilation is a prerequisite of renin release mediated by intracellular generation of cyclic AMP. To examine this hypothesis further the effects on renin release of theophylline, which would maintain high intracellular concentration of cAMP by inhibiting phosphodiesterase, were studied in anesthetized dogs. After inhibiting beta-adrenergic stimulation with propranolol, theophylline increased renin release significantly from 0.7 +/- 0.2 to 1.8 +/- 0.7 micrograms/min at control blood pressure and from 23 +/- 4 to 41 +/- 5 micrograms/min at a renal perfusion pressure of about 50 mmHg. The greater effect at low blood pressure occurred despite adjustment of the infusion rate of theophylline to keep arterial plasma concentration of theophylline unaltered. Isoproterenol infusion at low blood pressure raised renin release from 41 +/- 11 to 76 +/- 19 micrograms/min before and 54 +/- 13 to 108 +/- 31 micrograms/min during continuous infusion of theophylline. The renin release response to infusion of theophylline at low blood pressure was not enhanced by DB-cAMP infusion. We conclude that arteriolar dilation provides a condition for stimulation of renin release during the theophylline infusion. Theophylline infusion may augment the effect of isoproterenol on renin release by delaying the intracellular degradation of cAMP.
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PMID:Conditions for augmentation of renin release by theophylline. 631 54

Previous studies have shown that sympathetic factors and blood glucose are of importance in the development of seizures and lung damage from OHP. In the present study we examined the influence of beta sympathetic agonists and blocking agents and glucagon on OHP toxicity. Rats were exposed to 6 ATA OHP and examined for time-to-seizure and lung damage. Pretreatment with propranolol increased the time-to-seizure by 70% and practolol by 50% without altering gross lung appearance or lung wet wt/dry wt. Propranolol and practolol also prevented brain glycogen depletion prior to seizure which otherwise occurred in subconvulsive exposure to OHP. Isoproterenol and glucagon pretreatment had no effect on time-to-seizure but isoproterenol did increase lung injury. Both practolol and propranolol block the beta-receptor influence on adenyl cyclase-stimulated second messenger production, while both isoproterenol and glucagon activate adenyl cyclase to produce second messenger. Our results may suggest a possible role for second messenger in mediating some of the acute toxic effects of OHP on the CNS.
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PMID:Beta adrenergic receptors and glucagon in seizures from exposure to oxygen at high pressure (OHP). 631 53

We have shown previously that short-term nutritional deprivation causes a tissue-specific loss of liver ornithine decarboxylase (ODC) induction after isoproterenol, phenylephrine, or glucagon administration in rat pups. To examine the role of nutrition in the regulation of hepatic ODC, we tested the ability of intragastric nutrient administration to reverse nutritionally related deficits in the ODC response to hormonal challenge. Intragastric whole milk was effective in restoring ODC induction and accumulation of its immediate product, putrescine, in response to isoproterenol administration. Glucose was shown to mediate this effect by the ability of intragastric skimmed milk, lactose, galactose, or D-glucose to return ODC induction, and the inability of casein, sucrose, fructose, L-glucose, or pyruvate plus lactate to do so. D-Glucose also reestablished ODC induction by phenylephrine and glucagon. Parenteral administration of D-glucose produced results comparable to those obtained after intragastric administration. Isoproterenol induction of ODC was prevented when hepatic glucose uptake was blocked by phlorizin but not by blockade of central nervous system glucose uptake with 2-deoxyglucose. We conclude that intrahepatic glucose is an absolute requirement for hepatic ODC induction by isoproterenol, phenylephrine, or glucagon in preweanling rats.
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PMID:Intrahepatic glucose: a requirement for neonatal ODC induction by specific hormones. 638 Mar 9

In rats, the intravenous infusion with acebutolol lead to a dose dependent decrease of arterial blood pressure, heart rate, cardiac output and total peripheral resistance, to sinus bradycardia, widening of the QRS complex, 1st and 2nd degree AV-block and intraventricular conductance disturbances. Nine possible antidotes were administered i.v. to rats which had been infused with 2 mg/kg X min acebutolol for 60 min. Isoprenaline proved the best antidote against acebutolol antagonizing the bradycardia by 88% and the hypotension completely. The activities of orciprenaline and prenalterol were lower than those of isoprenaline. Dopamine, epinephrine and norepinephrine antagonized acebutolol-induced hypotension, but did not influence considerably the bradycardia. Glucagon, on the other hand, antagonized the acebutolol-induced bradycardia by 47% but exerted only a small activity on the hypotension. Aminophyllin and calcium were nearly ineffective as antidotes against acebutolol. Isoprenaline and dopamine infused simultaneously restored heart rate, arterial blood pressure and cardiac output of acebutol-poisoned rats. The survival time of rats infused with 4 mg/kg X min acebutolol was doubled by the additional infusion of 0.2 mg/kg X min isoprenaline. The antagonistic activity of a treatment with isoprenaline and dopamine against the cardiovascular toxicity of acebutolol was confirmed in rabbits.
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PMID:[Antidotal treatment of acebutolol poisoning]. 654 85

Rats anesthetized with pentobarbital and ventilated artificially were intoxicated with 1 mg/kg X min propranolol i.v. After 30 min heart rate, mean arterial blood pressure and peripheral resistance had dropped by about 50% and cardiac output by about 25% and were stable for up to 120 min. Isoprenaline proved to be the best antidote for the treatment of propranolol intoxication antagonizing the bradycardia by 76% and the hypotension completely. The antagonistic activities of orciprenaline and prenalterol were lower than those of isoprenaline. Dopamine, adrenaline and noradrenaline antagonized propranolol-induced hypotension but did not considerably influence the bradycardia whereas dobutamine was nearly ineffective in both respects. Glucagon and aminophylline displayed some chronotropic activity without influencing propranolol-induced hypotension. Calcium chloride, on the other hand, produced a moderate elevation of blood pressure but only a small chronotropic activity, and atropine was inactive in both respects. Isoprenaline also restored the cardiac function of propranolol-poisoned rats if administered by infusion and, furthermore, increased the lethal dose of propranolol from 77 to 165 mg/kg. The strong antagonistic activity of isoprenaline against propranolol-induced cardiovascular depression was also confirmed by experiments in pigs. In conclusion, isoprenaline is the most active antidote for the treatment of propranolol intoxication in the rat though the administration of massive doses are required. The vasodilatory effect of isoprenaline can be overcome by the additional administration of a vasoconstricting agent like dopamine.
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PMID:Evaluation of antidotes against the acute cardiovascular toxicity of propranolol. 674 Jul 1

Isoproterenol infusion increases renin release at low but not at control blood pressure. To examine whether this effect is dependent on arteriolar dilation and is specific for agonists of beta-adrenoceptors, responses to intrarenal infusion of isoproterenol (0.2 micrograms.kg body wt-1.min-1), glucagon (0.1 micrograms.kg body wt-1.min-1), and dopamine (1 micrograms.kg body wt-1.min-1) were compared at control and low or high ureteral pressure, which also dilates the renal arterioles. During renal arterial constriction, renin release was equal at two perfusion pressures below the range of autoregulation and was 76 +/- 24 micrograms/min higher during isoproterenol than during propranolol administration. Intravenous infusion of isoproterenol gave qualitatively similar results. Intrarenal infusion of glucagon and dopamine increased renin release by 13 +/- 3 and 22 +/- 12 micrograms/min, respectively; enhancement of renin release was also present after propranolol administration. During ureteral occlusion, intrarenal infusion of isoproterenol, dopamine, and glucagon increased renin release from 30-40 micrograms/min by 78 +/- 11, 13 +/- 3, and 31 +/- 10 micrograms/min, respectively. At control blood and ureteral pressure, the effects on renin release of infusing isoproterenol, dopamine, or glucagon were small or absent. Thus, isoproterenol, dopamine, amd glucagon enhance renin release when the arterioles are dilated by renal arterial constriction or ureteral occlusion.
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PMID:Conditions for enhancement of renin release by isoproterenol, dopamine, and glucagon. 703 49

The responses of hepatic glycogenolysis to catecholamines in ventromedial hypothalamus (VMH)-lesioned male rats were examined in perfused livers. Seven days after bilateral electrical lesioning of the VMH, the livers were perfused. Isoproterenol, a beta-agonist, stimulated greater glucose production in VMH-lesioned rats than in controls (32.8 vs. 5.6 mumol glucose.h-1.g liver-1), while responses to phenylephrine, an alpha-agonist, decreased significantly compared with controls (44.4 vs. 69.8 mumol glucose.h-1.g liver-1). There were no significant differences in responses of livers to glucagon and vasopressin between control and VMH-lesioned rats. Adrenodemedullation showed the same effect on beta-responses as lesions in the VMH, but no effect on alpha-responses. Plasma epinephrine levels were not detectable with the high-performance liquid chromatography analysis in VMH-lesioned rats. The periodicity of plasma corticosterone levels was observed in both VMH-lesioned and control rats, although daytime increases in plasma corticosterone were blocked by VMH lesions. These results suggest that the lesions in the VMH cause changes in the levels of adrenergic receptor and that the increase in beta-responses is caused mostly by the reduction of plasma epinephrine.
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PMID:Responses to catecholamines in perfused livers of hypothalamic-lesioned rats. 834 75


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