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)

Changes in glucagon, growth hormone (GH), cortisol, renin and aldosterone accompanying the metabolic disturbances and dehydration of severe diabetic ketoacidosis were studied over a 24 h period in eight patients treated with a constant intravenous insulin infusion. Mean steady state plasma-free insulin levels achieved were 28.6--49 mu/1 in patients receiving 2 u/h but a satisfactory rate of fall of glucose was not always obtained until the infusion dose was increased to 4 u/h or more. The total insulin dose administered was positively correlated with the level of plasma glucagon and cortisol on admission. During insulin infusion, both glucagon and cortisol fell but the rate of fall was not related to dose or plasma level of free insulin achieved. In six of eight patients studied increments in plasma GH above admission levels were observed during insulin treatment. Admission values of both plasma renin activity and plasma aldosterone were raised. The renin levels were highest in newly diagnosed diabetics, and two patients with long-established diabetes showed only small increments despite profound dehydration. Plasma renin activity, but not plasma aldosterone correlated with the fluid and sodium retention over the initial 24 h treatment period, but not with potassium requirements. The urinary excretion rates of the small molecular weight proteins GH and insulin, were considerably elevated over the treatment and convalescent periods.
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PMID:Hormonal responses during treatment of acute diabetic ketoacidosis with constant insulin infusions. 10 71

Infusion of 2 MRC/kg X h calcitonin in anaesthetised dogs produced a significant increase in plasma-renin activity, clearance of 51Dr-EDTA and 125I-o-iodohipuric acid, heart rate and urinary excretion of sodium, potassium, calcium and phosphates, while serum electrolytes and mean arterial pressure markedly fell. Infusion of 5 mug/kg X min glucagon produced a significant fall of plasma-renin, heart rate rose, but arterial mean pressure fell, and serum and urinary electrolytes did not change significantly, Cyclic AMP (dibutyryl-cAMP) significantly stimulated renin at a dose of 5 mg/min, while there were no significant changes in blood pressure, heart rate and serum and urinary electrolytes.
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PMID:[The effects of calcitonin, glucagon and the dibutyryl derivative of cyclic AMP on plasma-renin activity (author's transl)]. 18 47

Ten mug/min glucagon infused intravenously for 30 min in conscious dogs (weight 15-25 kg) is shown to increase renal prostaglandin activity and to produce a natriuretic effect, which is impaired by indomethacin pretreatment. Cardiac output, heart rate, renal blood flow and urine cAMP excretion are similarly increases in non-pre-treated and indomethacin pre-treated dogs. Glucagon infusion does not consistently change plasma renin activity in non-pre-treated dogs, while the renin secretion is almost totally blocked when glucagon is administered to dogs that are pre-treated with indomethacin. The results are consistent with the view that the natriuretic response to glucagon is largley dependent upon increased renal blood flow. An addition tubular prostaglandin mediated and possible anti-aldosterone effect is, however, also involved.
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PMID:Prostaglandin mediated natriuresis during glucagon infusion in dogs. 18 53

The effects of glucagon alone or in combination with theophylline on renin section were studied in relation to renal hemodynamic responses in anesthetized dogs. The intrarenal infusion of glucagon (0.5 microgram/kg/min) increased heart rate, renal blood flow, glomerular filtration rate and urine flow without any effect on renin secretion, but at a higher dose (1.0 microgram/kg/min) it increased renin secretion significantly. Theophylline (0.1 mg/kg/min) did not affect renal hemodynamics but caused a slight increase in renin secretion after 30--60 min infusion. The combined infusion of glucagon (0.5 microgram/kg/min) with theophylline (0.1 mg/kg/min) increased renin secretion markedly, although it produced renal hemodynamic changes similar to those induced by glucagon alone. These effects were not suppressed by d,l-propranolol (1.0 microgram/kg/min). It is suggested that the increase in renin secretion caused by the combined infusion of glucagon and theophylline resulted mainly from an increase in cyclic AMP in the juxtaglomerular cells, and not from stimulation of beta-adrenoceptors.
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PMID:Effect of glucagon on renin secretion in the dog. 21 14

Leading physical sign of "trauma-disease" in polytraumatized patients is hypovolemic shock. Changes in metabolism have been described previously. At present there are no reports concerning the time at which these changes occur. The early posttraumatic phase is characterized by normosodiemia and initial transient hypopotassemia, which is based on the renin-angiotensin-mechanism. The metabolic acidosis depending on trauma causes decreased oxygen perfusion of tissue, which possibly is found even before alterations of circulation are detected. Already at the site of the accident hyperglycemia and hyperglucagonemia with normal values of insulin were found. The increase of blood glucose was correlated to the values of adrenalin and to the insulin antagonist glucagon. The catabolism of proteins closely related to the degree of trauma continued as long as 5 days after injury. Analysis of the blood clotting system showed that in the early phase after trauma there are changes in hemostatic potential consisting in hemostatic defect. In several essential points the early posttraumatic phase of metabolism is different from that in a later phase. These facts should be kept in mind if planning therapy.
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PMID:[Metabolic changes in the multiply injured. Biochemical studies in multiply injured patients with reference to the severity of the injury]. 49 70

Suicidal attempt using beta-blockers are rare. Overdose by the ingestion of a large number of tablets rarely exceeds the high therapeutic doses suggested for the treatment of certain resistant cases of hypertension. The case described is that of a 65-year-old patient who took 800 mg of propanolol. Observation of plama levels showed that the half-life propanolol in the case of overdose is prolonged: 8.6 hours in this case, with a maximum plasma level of 1536 ng/ml. Plasma renin activity levels were low during the phase of intoxication and showed evidence of a rebound effect at its end. Treatment is above all that of the circulatory insufficiency produced: isopropylnoradrenaline or glucagon. Indications for extra-renal dialysis should take into account knowledge concerning the pharmacokinetics of these drugs and their prolonged physiological action.
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PMID:[Deliberate self-overdose with propranolol. Changes in serum levels (author's transl)]. 66 97

1. Isolated cat kidneys were perfused in situ with Locke solution and renin release in response to isoprenaline was studied. 2. Perfusion with isoprenaline produced a concentration-dependent enhancement of renin secretion. Increasing the concentration of stimulant also prolonged the duration of the secretory response. 3. After a 10 min exposure to isoprenaline (0-3 micrometer), there was a rapid facilitation of renin release which diminished after 10-30 min, followed by a second transient increase which declined over the next 40-60 min. Cycloheximide did not prevent augmented release when added together with the isoprenaline but did produce a reversible inhibition of the late phase when added 10 min after the isoprenaline. 4. Omission of calcium from the perfusion medium failed to depress the renin release induced by isoprenaline, glucagon, or furosemide. However, during prolonged calcium deprivation, the cycloheximide-sensitive phase of isoprenaline-evoked release was depressed. 5. The calcium antagonist D-600 failed to block the early phase of isoprenaline-induced renin secretion but inhibited the late phase of secretion. 6. Calcium alone elicited an explosive discharge of renin when added after a prolonged period of calcium-free perfusion. 7. These results support the view that extracellular calcium does not play an essential role in the mechanism of renin secretion from the renal juxtaglomerular cells, but that an increased influx of this cation is needed for synthesis and/or mobilization of the enzyme. It is tentatively proposed that the release of calcium from intracellular storage sites may be the signal which triggers renin secretion.
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PMID:The role of calcium in renin secretion from the isolated perfused cat kidney. 89 93

The effect of cycloheximide, an inhibitor of protein synthesis, on basal and stimulated renin secretion was examined in the isolated perfused rat kidney. Cycloheximide (0.05 mmol) was administered one hour before preparing the kidneys for perfusion. Both basal renin secretion and the response to intrarenal infusion of isoprenaline (0.06 nmol/min/g) or glucagon (0.1 nmol/min/g) were consistently reduced in the cycloheximide-treated group, suggesting dependence of these processes on protein synthesis.
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PMID:Suppression of renin secretion in the isolated rat kidney by cycloheximide. 99 24

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

Administration of 0.2 mg of glucagon by intravenous bolus resulted in an increase in plasma renin activity (PRA) in 2 of 5 normal volunteers on their usual diet. Two of the nonresponders subsequently showed a PRA response to glucagon after sodium depletion. A lower dose of glucagon (0.01 mg) had no effect on PRA despite a 31 mg/100 ml rise in blood glucose and peak plasma glucagon of over 2000 pg/ml. In conclusion, glucagon can stimulate PRA but it is not a potent stimulator; its effect may be potentiated by sodium depletion.
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PMID:Glucagon stimulation of plasma renin activity in humans. 115 Aug 61


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