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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The effects of lanthanum on renin release and renal vasoconstriction were studied in the isolated perfused rat kidney. 2. Lanthanum reduced noradrenaline-induced renal vasoconstriction. 3. Lanthanum prevented isoprenaline-induced and glucagon-induced stimulation of renin secretion.
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PMID:Blockade of renin release by lanthanum. 107 84

Eight men were studied during graded (47, 77, and 100% of maximal oxygen uptake) and prolonged (76%) exhaustive treadmill running. During graded exercise the glucagon concentration increased 35% from 81 plus or minus 7 pg/ml (mean and SE) at rest to 109 plus or minus 17 after the heaviest load. During prolonged exercise glucagon increased progressively to three times (226 plus or minus 40) the resting value. Norepinephrine increased from 0.40 plus or minus 0.06 ng/ml to 2.22 plus or minus 0.39, epinephrine from 0.07 plus or minus 0.01 to 0.42 plus or minus 0.13 during graded, and to 1.51 plus or minus 0.08 and 0.33 plus or minus 0.04, respectively, during prolonged exercise. Insulin concentrations were depressed during work except for the heaviest load. Fatty acids rose throughout prolonged exercise, whereas blood glucose significantly diminished 30 min afterward. Glucagon concentrations correlated significantly with norepinephrine and epinephrine concentrations during prolonged and with epinephrine during graded exercise. Although increments in catecholamines were similar, the glucagon secretion was larger during prolonged than during graded exercise. While increments in catecholamines might explain increased glucagon secretion during graded exercise, they cannot account completely for the rise of glucagon during prolonged exercise.
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PMID:Glucagon and plasma catecholamine responses to graded and prolonged exercise in man. 111 Feb 46

Highly significant (P smaller than 0.0025) increases in adenylate cyclase activity were seen at all fetal age periods (5-17 weeks) whenever sodium fluoride (5-10 mM) was added to the enzyme prepared from human myocardium. Norepinephrine (NE) at 10-4 M significantly elevated adenylate cyclase activity commencing at 6-7 weeks (P smaller than 0.01). Beginning at 8-9 fetal weeks, glucagon (6x10-6 M) effectively activated adenylate cyclase. Other hormonal agents, namely, histamine, epinephrine, and isoproterenol at 10-4 M, demonstrated an ability to activate the enzyme (P smaller than 0.025) by as early as 6-7 weeks and continued to act in this manner throughout the remainder of the developmental periods investigated. The beta blocking agents, propranolol, significantly inhibited (P smaller than 0.25) the stimulation of adenylate cyclase by NE throughout the 8-15 fetal week periods.
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PMID:Appearance of hormone-sensitive adenylate cyclase in the developing human heart. 111 98

1. Variations in the output of glucocorticoids and catecholamines from the right adrenal gland, in response to insulin hypoglycaemia, have been investigated in calves 2-5 weeks after birth. These have been correlated with changes in the concentration of glucocorticoids and glucagon in arterial plasma. 2. Moderate hypoglycaemia for a limited period (0-1 u. insulin/kg), elicited a prompt increase in steroid output from the adrenal gland followed by a significant rise in plasma glucagon concentration. By comparison, changes in both catecholamine output and peripheral plasma glucocorticoid concentrations were found to be trivial in this group of animals. 3. Administration of a larger dose of insulin (0-5 u./kg) produced a more substantial fall in plasma glucose concentration followed by spontaneous recovery within 2-3 hr. This stimulus elicited the release of greater amounts of both cortisol and corticosterone, followed by a significant increase both in the output of adrenaline and in plasma glucagon concentration. Increase in steroid output was accompanied by an increase in adrenal blood flow and was associated with elevated concentrations of both steroids in arterial plasma. 4. The adrenal cortical response and associated changes in plasma steroid concentration were found to be transient even in response to persistent and intense hypoglycaemia (4 u. insulin/kg). The increase in plasma glucagon concentration in this group of animals was not significantly greater than that produced by smaller doses of insulin. However, substantial amounts of adrenaline (78 plus or minus 14 ng. kg-minus 1 min-minus 1; maximum; n equals 9) together with a little noradrenaline (10 plus or minus 3 ng.kg-minus 1 min-minus 1; maximum; n equals 9) were released from the right adrenal gland under these conditions. 5. Changes in adrenal blood flow could be related to adrenal glucocorticoid output in calves given 0-1 or 0-5 u. insulin/kg. In animals given the largest dose of insulin adrenal blood flow was found to increase coincidentally with rising steroid output but this hyperaemia then persisted after steroid output had subsided to values within the normal range. 6. Calves given the largest dose of insulin (4-0 u./kg) invariably collapsed and convulsed after 2-3 hr, but these symptoms could not be related to any particular endocrine response. No clinical signs of hypoglycaemia were observed in the other animals. 7. The results are discussed in relation to previous studies of adrenal function in this and other species.
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PMID:Endocrine responses to insulin hypoglycaemia in the young calf. 113 79

Studies were performed in 6 healthy, male volunteers to explore the effect of a work load on the blood concentrations of catecholamines in relation to pulse rate and blood pressure and the blood levels of pancreatic glucagon, insulin, growth hormone, glucose and glycerol. The work load consisted of 300 kpm/min for 5 min, followed by 600 kpm/min during the next 5 min and 900 kpm/min under a third 5 min period. The work load resulted in a marked increase in noradrenaline and adrenaline at 10 and 15 min of exercise. The pulse rate, the systolic pressure and the mean blood pressure were correlated to the blood levels of both adrenaline and noradrenaline. In spite of the rather marked activation of the sympathetic nervous system no increase occurred in glucagon as measured under exercise and up to 60 min after its completion. In 4 of the subjects the work load was followed by a prompt growth hormone response. The same 4 subjects also showed a marked increase in catecholamines. The 2 remaining subjects presented no change in growth hormone and their increase in catecholamines was relatively minor. Glycerol increased significantly during work and there was a positive correlation between the values recorded for glycerol and adrenaline. No significant changes occurred in blood sugar or insulin during work.
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PMID:The influence of short term submaximal work on the plasma concentrations of catecholamines, pancreatic glucagon and growth hormone in man. 117 88

Glucagon in small intravenous (i.v.) doses markedly increases glomerular filtration rate (GFR) in normal anesthetized dogs. In this study, the effects of glucagon 5 mug/min (i.v.) on renal hemodynamics was tested in four canine models of acute pre-renal failure (hemorrhage, barbiturate overdose; renal arterial clamping and renal arterial infusions of noradrenaline) and in a model of unilateral acute tubular necrosis at 4 h and 6-7 days following completion of the ischemic insult. Following hemorrhage and barbiturate excess, with arterial blood pressure maintained at 65-70 mm Hg, whole-kidney GFR and clearance rate of p-aminohippurate decreased by 50-70%. During this reduction of perfusion pressure, the subsequent infusion of glucagon increased GFR by 90-130%. In models where arterial pressure was normal during the period of ischemia (clamping and noradrenaline infusion), not only did glucagon significantly increase renal perfusion, but the ischemic kidney proved to be far more sensitive to the hemodynamic effects of glucagon (delta GFR - 120-160%) than the contralateral control (deltaGFR = 30-40%). In three dogs completely anuric following renal arterial clamping, glucagon was able to improve blood flow and restart urine formation. Glucagon, but not dopamine, was able to simulate the beneficial effects of hypertonic mannitol on renal function in dogs with hemorrhagic hypotension. Glucagon was without effect in established acute tubular necrosis. This study, therefore, indicates that, during renal ischemia, glucagon may be quite effective in preserving urine output and perfusion of the kidneys.
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PMID:The effect of glucagon on glomerular filtration rate in dogs during reduction of renal blood flow. 117 90

In order to analyze separately the effects of cell size and age on the metabolism of rat adipose tissue, fat cells of different sizes were obtained from the same animals. The rats were 4 or 15 wk old. The results show that age as well as cell size influences the metabolic rates. At a given cell size, the basal lipolysis, the lipolytic effects of glucagon and noradrenaline, the rate of glucose incorporation into the triglycerides, and the effect of insulin on glucose metabolism were considerably increased in the young animals. Furthermore, irrespective of fat cell size the lipolytic action of glucagon was reduced in old animals. The data thus show that experiments with large fat cells from old rats and with small cells from young animals cannot be directly compared because both variables may influence metabolic reactions.
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PMID:Effects of age and cell size on rat adipose tissue metabolism. 119 89

Significant increases in mean plasma noradrenaline levels were observed 30-60 min and 150-180 min after a subcutaneous injection of 1 mg glucagon. The first peak coincided with the maximum blood glucose and plasma insulin levels and the second peak occurred after plasma growth hormone (GH) and cortisol levels had begun to rise. The first plasma noradrenaline peak may be important in inhibiting further insulin secretion. There was no evidence that glucagon stimulates adrenaline secretion in normal human subjects. It was also confirmed that there are significant increases in the levels of glucose, insulin, GH and cortisol and a significant decrease in FFA levels following subcutaneous injection of glucagon in normal human subjects.
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PMID:The metabolic and hormonal response to glucagon. Part 1. Normal subjects. 126 1

The hormonal and metabolic changes following the subcutaneous injection of 1 mg glucagon have been studied in a group of 6 migraine patients, and the results indicate that the responses of these subjects differ from those of a control group. Three of the migraine subjects had raised basal plasma noradrenaline levels but all had been taking clonidine up to 12-24 hr before the test and the increased plasma noradrenaline levels were probably due to the effect of withdrawal of the drug.
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PMID:The metabolic and hormonal response to glucagon. Part 2. In patients with migraine. 126 2

1 The hepatic artery of the anaesthetized dog was cannulated and perfused from a femoral artery, the blood flow and perfusion pressure being monitored continuously. The sympathetic periarterial nerves were divided. 2 Dose-dependent increases in hepatic arterial vascular resistance (HAVR) resulted from intra-arterial injections of noradrenaline, angiotensin and vasopressin. 3 Single injections of glucagon (100 mug, i.a.) caused a transient significant fall in HAVR of 19.9 +/- 3.2%, and infusions of 25 mug/min of glucagon intra-arterially caused maintained reductions in HAVR of 16.9 +/- 4.2%. 4 After single injections of 100 mug glucagon intra-arterially the vasoconstrictor responses to noradrenaline, angiotensin, and vasopressin were reduced by about 85-95%. Recovery occurred in 8-10 minutes. 5 Intra-arterial infusions of glucagon, 2.5-50.0 mug/min, reduced the effects of test doses of noradrenaline, angiotensin and vasopressin throughout the period of the infusions. 6 Dose-response curves to the constrictor agents were constructed before, during and after intra-arterial infusions of 25 mug/min of glucagon. Glucagon caused a parallel shift of the curves for noradrenaline and angiotensin to the right, with no suppression of the maximum response. 7 Infusions of glucagon shifted the dose-response curve for vasopressin to the right, but, in contrast to noradrenaline and angiotensin, the shift was nonparallel and there was a suppression of the maximum response by about one-half. 8 A large dose of insulin, 10 iu, transiently reduced HAVR and caused a weak and very transient inhibition of the effect of test doses of noradrenaline. The characteristics of these effects were quite different from those of glucagon. 9 It is possible that the antagonism by glucagon of the vasoconstrictor responses of the hepatic arterial vasculature may be important in protecting this vascular bed from the effects of concomitantly released vasoconstrictor agents.
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PMID:The inhibition by glucagon of the vasoconstrictor actions of noradrenaline, angiotensin and vasopressin on the hepatic arterial vascular bed of the dog. 127 44


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