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)

Clearance studies were performed in 23 dogs undergoing extracellular volume (ECV) expansion by saline in order to evaluate relationship between endogenous glucagon and renal excretion of sodium and calcium. In control animals plasma glucagon (pG1) rose following 120 minutes of ECV expansion and was further increased by additional infusion of arginine. In pancreatectomised dogs ECV expansion failed to increase pG1. Both fractional and absolute urinary excretion of sodium in pancreatectomised dogs were markedly lower compared to control dogs. The difference in renal sodium excretion between control and pancreatectomised animals cannot be explained by the sum of nonhormonal factors influencing sodium excretion. In thyro-parathyroidectomised dogs renal sodium excretion was lower than in control dogs, but significantly higher than in pancreatectomised dogs. The arginine-induced increase of glucagon was associated with an increase of renal sodium and calcium excretion in each group under study without any change in glomerular filtration rate. In control dogs all parameters of renal sodium and calcium excretion investigated in this study were linearly correlated. Thyro-parathyroidectomy did not influence the relationship between renal sodium and calcium excretion. Hyperglucagonaemia therefore might be one factor contributing to the hypercalciuria associated with renal stone formation. In pancreatectomised dogs undergoing ECV expansion there was no significant correlation between renal sodium and calcium excretion. Pancreatic hormones might be involved in the coupling of renal sodium and calcium excretion.
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PMID:Urinary sodium and calcium in various dog models and relationship to endogenous plasma glucagon. 87 3

A rise in glomerular filtration rate (GFR) during saline infusion increases outer medullary more than cortical metabolic rate. To determine whether other GFR-increasing agents have a similar effect, renal metabolic rates were estimated by the heat-production technique during infusion of glycine or glucagon. Glycine and glucagon increased GFR by 17 +/- 2 and 32 +/- 2%, renal blood flow (RBF) by 34 and 21%, and outer medullary metabolic rate by 42 +/- 3 and 59 +/- 4%, respectively. Cortical metabolic rate rose by 7 +/- 1% during glucagon, and it increased by 29 +/- 2% during glycine infusion, suggesting a stimulation unrelated to sodium reabsorption. To determine whether glucagon influenced renal metabolism independent of its GFR-increasing effects, vasodilation was achieved by ureteral or suprarenal aortic constriction. Glucagon was without effect on RBF, GFR, and metabolic rate, but infusion of acetylcholine still raised RBF. We conclude that glucagon increases GFR by dilating vascular segments participating in autoregulation, and that energy-requiring NaCl reabsorption in the outer medulla is increased secondary to increased delivery of NaCl.
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PMID:Effect of glycine and glucagon on glomerular filtration and renal metabolic rates. 87 23

This experimental study was conducted to compare and contrast the cardiovascular effects of the drugs most commonly used to alleviate low-cardiac-output syndrome. Twenty-five adult mongrel dogs were infused with sodium pentobarbital (60 mg/min) until their cardiac output fell to 50+/-5% of the average control values determined by thermodilution technique prior to pentobarbital infusion. The dogs were then divided into six groups, and one of the following agents or combinations of agents was administered to each group: isoproterenol, glucagon, dopamine, dobutamine, levarterenol and phentolamine, or levarterenol and nitroprusside. All drugs, except for glucagon and the combination of levarterenol and nitroprusside, produced an increase in cardiac output above the nonfailure baseline values. However, this increase was accompanied by an undesirable, pronounced tachycardia except when levarterenol was used simultaneously with phentolamine. Both dopamine and the combined infusion of levarterenol and phentolamine proved the most effective in restoring systemic arterial pressure to near baseline values, and both were able to increase renal blood flow above the failure baseline values. While renal blood flow remained elevated with all dosages of levarterenol and phentolamine, it tended to decrease with larger doses of dopamine. These experiments demonstrate that there are major advantages in the use of simultaneously infused levarterenol and phentolamine for control of low-cardiac-output syndrome: increased cardiac output without elevated peripheral vascular resistance, restoration of systemic arterial pressure and consequent improved coronary flow, absence of tachycardia, and augmented renal blood flow.
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PMID:A comparison of the hemodynamic effects of inotropic agents. 93 38

Unidirectional K+ fluxes were measured in suspensions of isolated rat liver parenchymal cells incubated with 42K+ in vitro. By tracer exchange analysis fluxes in both directions were estimated to 8-9 10(-12) mol/cm2. Glucagon in concentrations above 2 x 10(-8) M increased both influx and efflux to 160% of control values. Insulin increased influx by 12-14%, whereas efflux was apparently unaffected. Using an extracellular marker 51Cr EDTA, intracellular level of some ions was estimated in isolated liver cells: K+ = 172 mmol/kg water, Na+ = 25 mmol/kg water, Cl = 53 mmol/kg water. Cellular water content: 60%. Incubation with insulin for 1 h increased the intracellular concentration of K+ 1.7 mmol/kg water. The results indicate that glucoagon increased primarily the K+-permeability of the cell membrane, while insulin stimulates active K+ transport into the cell.
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PMID:K+ transport in isolated rat liver cells stimulated by glucagon and insulin in vitro. 94 6

1. Isolated lamb liver cells were prepared from 24-h-starved animals by venous perfusion of the excised caudate lobe with buffer containing collagenase. On the basis of Trypan-Blue exclusion, rate of O2 uptake, adenine nucleotide content and retention of constitutive enzymes, these cells were judged to be intact. 2. Isolated caudate-lobe liver cells showed rates of gluconeogenesis from 10 mM-propionate and 10 mM-lactate that compared favourably with rates determined in isolated median-lobe cells and with rates determined with the isolated perfused lamb liver. 3. The gluconeogenic potential of substrates tested depended on the lamb's age. Cells prepared from suckling lambs (up to 20 days of age and essentially non-ruminant) showed highest rates from galactose, serine and alanine; those prepared from post-weaned lambs (older than 30 days of age and ruminant) showed highest rates from propionate, lactate and fructose. 4. Gluconeogenic rates from endogeneous precursors, 10 mM-propionate and 10mM-galactose, were linear for 1 h and were both stimulated by 1 muM-glucagon. Provided the endogenous rate of gluconeogenesis remained unchanged after substrate addition, glucagon caused a net stimulation of gluconeogenesis from each of these substrates. 5. Gluconeogenic capacity and glucagon sensitivity were examined in cells maintained in substrate-free oxygenated buffer at 37 degrees, 22 degrees and * degrees C. Even under the best of the three conditions of storage that were tested (i.e. at 22 degrees C in gelatin-containing buffer) deterioration of the lamb cells proceeded rapidly, and loss of glucagon responsiveness preceeded the loss of ability to convert precursor into glucose. 6. n-Butyric acid, 2-methylpropanoic acid and 3-methylbutanoic acid at concentrations comparable with those found in lamb portal-vein blood each stimulated gluconeogenesis from 10mM-galactose or 10mM-propionate; gluconeogenesis from galactose was stimulated to the greater extent. 7. The regulatory effects of glucagon and sodium butyrate on lamb liver-cell gluconeogenesis and glycogenolysis were compared. Glucagon (1 muM) and 2mM-butyrate accelerated the rate of glucose formation of liver cells of 24h-starved animals from lactate+pyruvate or fructose. Insulin (20nM) decreased both gluconeogenesis and the efficacy of 1 muM-glucagon. For lactate+pyruvate as substrate, the stimulatory effect of butyrate was additive to that of 1muM-glucagon and for both lactate+pyruvate and fructose the stimulatory effect of butyrate was not influenced by 20nM-insulin. In contrast with glucagon, which stimulated the rate of glycogenolysis in cells prepared from fed lambs, butyrate (0.1-20mM) had no effect. 8. It is concluded that glucagon and butyrate stimulate lamb liver-cell gluconeogenesis by different mechanisms.
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PMID:Gluconeogenesis in isolated intact lamb liver cells. Effects of glucagon and butyrate. 94 49

Endogeneous hyperglucagonemia is observed in experimental diabetes mellitus and semistarvation, conditions associated with an increased intestinal absorptive function. To examine whether glucagon might exert a similar adaptive response on intestinal digestive-absorptive function like experimental diabetes mellitus the effect of chronic glucagon administration on intestinal transport of 3-0-methyl-D-glucose, water, sodium, potassium, and D-glucose induced transmural potential difference (PD) was examined by an in vivo perfusion technique in rat small intestine. Chronic administration of glucagon (100 mug twice daily) for 5 days resulted in increased absorption of 3-0-methyl-D-glucose, water, sodium and potassium as well as in an increase of D-glucose induced PD. A similar, but more pronounced augmentation of D-glucose induced PD was observed in the jejunum of streptozotocin-diabetic rats. Disaccharidase (maltase, sucrase, trehalase, lactase) and alkaline phosphatase activities were not affected in intestinal mucosa of glucagon-treated rats compared to controls. It cannot be decided from these results whether hyperglucagonemia is responsible for the adaptive intestinal changes observed in experimental diabetes mellitus.
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PMID:Effect of chronic glucagon-administration on the digestive and absorptive function of rat small intestine in vivo. 98 1

The effect of intravenous injection of 50 mug/kg of glucagon on the hepatic circulation of the pig was studied in 12 animals. Glucagon caused an arterial pressure reduction of 11 mm Hg after two minutes and 7 mm Hg after ten minutes. The portal pressure and blood flow were not altered. The superior mesenteric arterial flow decreased by 12%. The hepatic arterial blood flow increased by 80% after two minutes and by 58% after ten minutes. There was no difference in response when anesthesia was achieved with small intravenous doses of thiopental (Pentothal) sodium or 70% nitrous oxide in oxygen and tubocurarine chloride.
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PMID:Effect of glucagon on hepatic circulation in the pig. 99 4

Tumoral secretions and pathophysiology of diarrhea were studied in 1 patient with pancreatic cholera. High concentrations of vasoactive intestinal peptide were found in both systemic blood and tumoral extracts, together with increased plasma levels of calcitonin and protaglandins E and Falpha. Gastric inhibitory peptide and gastrointestinal and pancreatic hormones were absent from the tumor, except for small amounts of glucagon, and their blood levels were normal. Decreased basal but normal pentagastrin-stimulated gastric acid secretion, normal basal and secretin-stimulated pancreatic secretion, increased volume of gallbladder bile with high bicarbonate, and low bile salt concentrations were observed, but the electrolyte content and flow rate of fluid passing the duodenojejunal junction were within normal limits. Small intestine was found to be the origin of the water and electrolyte fasting losses. Jejunum was the site of bicarbonate secretion. Jejunal glucose and leucine-stimulated water and sodium transports were also strikingly decreased, whereas the absorption rates of the sugar and amino acid were normal. Colon reabsorbed high amounts of water and sodium but increased potassium losses. Biological effects of vasoactive intestinal peptide may explain most of the patient's upper digestive secretion abnormalities and small intestinal function impairments, whereas secondary aldosteronism might explain the modified colonic function.
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PMID:Pancreatic cholera. Sudies on tumoral secretions and pathophysiology of diarrhea. 109 88

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

The effects of insulin on the renal handling of sodium, potassium, calcium, and phosphate were studied in man while maintaining the blood glucose concentration at the fasting level by negative feedback servocontrol of a variable glucose infusion. In studies on six water-loaded normal subjects in a steady state of water diuresis, insulin was administered i.v. to raise the plasma insulin concentration to between 98 and 193 muU/ml and infused at a constant rate of 2 mU/kg body weight per min over a total period of 120 min. The blood glucose concentration was not significantly altered, and there was no change in the filtered load of glucose; glomerular filtration rate (CIN) and renal plasma flow (CPAH) were unchanged. Urinary sodium excretion (UNaV) decreased from 401 plus or minus 46 (SEM) to 213 plus or minus 18 mueq/min during insulin administration, the change becoming significant (P smaller than 0.02) within the 30-60 min collection period. Free water clearance (CH2O) increased from 10.6 plus or minus 0.6 to 13 plus or minus 0.5 ml/min (P smaller than 0.025); osmolar clearance decreased and urine flow was unchanged. There was no change in plasma aldosterone concentration, which was low throughout the studies, and a slight reduction was observed in plasma glucagon concentration. Urinary potassium (UKV) and phosphate (UPV) excretion were also both decreased during insulin administration; UKV decreased from 66 plus or minus 9 to 21 plus or minus 1 mueq/min (P smaller than 0.005), and tupv decreased from 504 plus or minus 93 to 230 plus or minus 43 mug/min (P smaller than 0.01). The change in UKV was associated with a significant reduction in plasma potassium concentration. There was also a statistically significant but small reduction in plasma phosphate concentration which was not considered sufficient alone to account for the large reduction in UPV. Urinary calcium excretion (UCaV) increased from 126 plus or minus 24 to 200 plus or minus 17 mug/min (P smaller than 0.01). These studies demonstrate a reduction in UNaV associated with insulin administration that occurs in the absence of changes in the filtered load of glucose, glomerular filtration rate, renal blood flow, and plasma aldosterone concentration. The effect of insulin on CH2O suggests that insulin's effect on sodium excretion is due to enhancement of sodium reabsorption in the diluting segment of the distal nephron.
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PMID:The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man. 112 Jul 86


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