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)

Glucagon (21.5 +/- 0.23 ng/min/kg) was infused through the portal vein of normal or pancreatectomized dogs. It was observed that a dose of glucagon that produces no significant change in the glycemia of normal dogs has a very small activity in the production of glomerulopressin and does not alter glomerular filtration rate (GRF). In pancreatectomized dogs this same dose of glucagon also does not alter glycemia but it induces a large increase in the production of glomerulopressin and GFR. Our results suggest that in pancreatectomized dogs glomerulopressin production is more sensitive to glucagon infusion than in normal dogs.
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PMID:Effect of glucagon on glomerulopressin production in diabetic dogs. 55 36

In anesthetized mongreal dogs, the intrarenal arterial (0.2 approximately 1.0 unit/kg-min) and the intravenous infusion (0.4 approximately 2.0 unit/kg-min) of secretin caused dose-dependent increase of RBF, accompanied by decreases of the calculated afferent arteriolar resistance (Ra) and efferent arteriolar resistance (Re), but produced no significant effect on GFR, urine flow, electrolyte excretion, osmolar clearance and free water reabsorption. The distribution of cortical blood flow was examined using the radioactive microsphere technique. The intrarenal infusion of secretin (1.0 unit/kg-min) increased renal cortical blood flow in the juxtamedullary area much more than in the superficial area, shifting the blood flow from the outer to the inner zone. Simultaneous intrarenal infusion of secretin (1.0 unit/kg-min) and glucagon (0.5 microng/kg-min) produced increases in GFR, urine flow and electrolyte excretion to a lesser degree than those induced by glucagon alone, whereas the increment in RBF and the decreases in Ra and Re were almost to the same degree as those caused by secretin alone. The present results indicate that secretin produces the dilation of afferent and efferent arterioles, resulting in an increase in RBF, with no change in GFR and urine flow, and that the effects of glucagon on renal functions are masked by secretin mainly through the effects of renal hemodynamics.
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PMID:[Effects of secretin on renal functions in the dog]. 55 40

The influence of glucagon on renal function and hemodynamics was studied on isolated perfused rat kidneys. During perfusion with solutions containing no vasoactive substances glucagon increased total renal perfusion flow, while the GFR remained unchanged. The autoregulation of blood flow under these conditions was completely abolished. Na-excretion was slightly reduced under the action of glucagon, due to an increased fractional Na-reabsorption. However, increased fractional Na-reabsorption was not due to a direct influence of glucagon on tubular transport mechanism as comparison of TNa at identical Na-loads demonstrated. In presence of angiotensin II renal perfusion flow was markedly reduced and doubled almost after starting glucagon infusion. GFR under these conditions rose by about 100%. It is concluded from the results that changes of kidney function following glucagon infusion are mainly due to a reduced vascular resistance.
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PMID:Glucagon induced functional changes of isolated perfused rat kidney. 61 76

Our study indicates that in renal failure elevated plasma triglyceride can first be detected when the GFR falls to 50 ml/min. Hypertriglyceridemia is the commonest abnormality found and increases further when the GFR falls below 10 ml/min. Plasma cholesterol levels remain normal even at low levels of renal function. Although plasma growth hormone, glucagon, and insulin levels become elevated when renal function diminishes, there is no definite correlation of their levels and GFR. A decreased incidence of hyperlipidemia observed in patients sustained by maintenance hemodialysis for over 5 yrs may in part be due to the triglyceride lowering effect of growth hormone and glucagon and/or the cholesterol lowering effect of insulin.
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PMID:Uremic hyperlipoproteinemia: correlation with residual renal function and duration of maintenance hemodialysis. 91 Mar 86

The effect of glucagon on the renal hemodynamics in the dog was examined by comparing its effect with that of secretin, a peptide with which glucagon shares a similar chemical structure. An intrarenal infusion of glucagon resulted in increases of RBF and GFR. GFR rose by approximately the same order of magnitude of RBF. The increase in GFR depended on the selective dilation of the afferent arteriole and a consequent rise in the transcapillary pressure difference. On the other hand, secretin infusion produced highly significant and proportional decreases in both afferent and efferent arteriolar resistance, resulting in no change in GFR. A superimposition of acetylcholine to glucagon decreased GFR even though RBF increased significantly. Glucagon infusion did not affect the permeability of glomerular capillary and the distribution of cortical blood flow. These findings indicate that the effect of glucagon on GFR depended on the selective dilation of afferent arteriole, and that as a result of its dilation the net filtration pressure increased without any change in permeability of glomerular capillary and a redistribution of filtration.
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PMID:Effects of glucagon on the renal hemodynamics in the dog. 91 58

The mechanisms underlying the renal hemodynamic responses (vasodilation and hyperfiltration) to an amino acid or protein load are currently unknown and are relevant to understanding the effect of dietary protein on the progression of chronic renal failure. Glucagon (GLC) has been suggested to be important in these renal hemodynamic responses, although the mechanism is again unclear. Thus we investigated potential mediators of the renal hemodynamic response to GLC in the anesthetized rat, including prostanoids and endothelium-derived relaxing factor (EDRF). The effects of glucagon alone and after pretreatment were tested as follows: (1) after baseline renal hemodynamic measurements done with clearance techniques, rats were given GLC alone (n = 5; 200 ng/min IV continuous infusion); (2) glucagon was given after pretreatment with the EDRF synthesis inhibitor nitro-arginine-methyl-ester (NAME; n = 6; 125 micrograms/kg/min intrarenal artery by continuous infusion); (3) glucagon was given after pretreatment with indomethacin (INDO; n = 6; 5 mg/kg IV bolus). Repeat clearances demonstrated that GLC infusion increased glomerular filtration rate (GFR; basal vs GLC, 0.87 +/- 0.04 ml/min vs 1.14 +/- 0.09 ml/min, p < 0.05); renal plasma flow (RPF; 4.10 +/- 0.18 ml/min vs 5.56 +/- 0.32 ml/min, p < 0.05) and decreased renal vascular resistance (RVR; 15.82 +/- 1.17 mm Hg/[ml/min] vs 10.72 +/- 0.65 mm Hg/[ml/min], p < 0.05). Intrarenal N-nitro-L-arginine-methyl-ester (NAME) infusion significantly reduced basal GFR (-20% +/- 8%, p < 0.05) and RPF (-43% +/- 2%, p < 0.05), while increasing RVR (+108% +/- 9%, p < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mechanisms of glucagon-induced renal vasodilation: role of prostaglandins and endothelium-derived relaxing factor. 145 14

We investigated the tubular action of endothelin in rat nephron segments. The effects of endothelin on arginine vasopressin (AVP)-, parathyroid hormone-, glucagon-, calcitonin-, and isoproterenol-dependent cAMP accumulation were studied. The following nephron segments were microdissected: glomerulus (Gl), proximal convoluted tubule (PCT), cortical and medullary thick ascending limbs of Henle's loop (cTAL and mTAL, respectively), cortical collecting duct (CCD), outer medullary collecting duct (OMCD), and inner medullary collecting duct (IMCD). Endothelin dose dependently (10(-8)-10(-10)M) inhibited AVP-dependent cAMP accumulation in CCD, OMCD, and IMCD. This effect was independent of the presence or absence of phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, Ca channel blocker nicardipine, or indomethacin, but was abolished in the presence of protein kinase C inhibitor H-7. Protein kinase C stimulator dioctanoyl glycerol mimicked the effect of endothelin. On the other hand, endothelin had no inhibitory effect on AVP-dependent cAMP accumulation in cTAL or mTAL, parathyroid hormone-dependent cAMP accumulation in Gl and PCT, or glucagon-, calcitonin-, and isoprotereol-dependent cAMP accumulation in OMCD. We conclude that endothelin specifically inhibits AVP-dependent cAMP accumulation in CCD, OMCD, and IMCD through activating protein kinase C. This effect possibly has a role in maintaining urine volume to counteract the decrease in GFR caused by endothelin itself.
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PMID:Effects of endothelin on peptide-dependent cyclic adenosine monophosphate accumulation along the nephron segments of the rat. 169 79

Ten patients with chronic renal failure (GFR 29-97 ml/min), on free diets providing 1 g/kg B.W. of proteins, ingested an oral protein load (meat meal, 2 g/kg B.W.). GFR and RPF increased significantly over baseline with no change in filtration fraction. Within 30 min of the meal and for the next 3 h a statistically significant increase was observed in the plasma concentrations of the following amino acid groups: essential, non-essential, total, branched-chain, ketogenic, glycogenic, glycogenic and ketogenic, basic, acid, polar and non-polar. At 30 min the smallest increase was seen in acid and polar amino acids (6.7% and 7.6%, respectively). At 180 min the largest increase (78.8%) was seen for glycogenic and ketogenic amino acids and total plasma amino acids were 1.58 times baseline. After the meat meal plasma glucagon and insulin rose significantly, while growth hormone, plasma renin activity and aldosterone did not vary.
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PMID:Renal hemodynamics, plasma amino acids and hormones after a meat meal in progressive nephron loss. 204 91

Renal functional reserve capacity was evaluated in 19 normotensive type I diabetics without microalbuminuria. All patients had normal basal renal function as assessed by 24-hour creatinine clearances higher than 120 ml/min. PAH, inulin, and creatinine clearances were carried out every hour before, during, and after infusion of an amino acid (AA) solution. The same experiment was repeated after ACE inhibition with captopril (25 mg). Two groups of patients were found: Group A (responders) showed a significant rise in GFR after AA infusion (inulin clearances from 117 +/- 8 to 138 +/- 10 ml/min) (p less than 0.05), whereas in Group B (non-responders) no significant change in GFR was observed. Groups were comparable in age, duration of diabetes, metabolic control, and mean arterial blood pressure. Group B, however, had a significantly higher basal inulin clearance (167 +/- 17 ml/min) than Group A (117 +/- 8 ml/min). In Group A ACE inhibition completely blocked the AA-induced rise in GFR, while basal GFR in Group B was significantly reduced (167 +/- 17 to 148 +/- 8 ml/min) after captopril administration. In both groups renal plasma flow was enhanced by ACE inhibition. A rise in glucagon was observed in all patients during AA infusion. It is concluded that type I diabetics with normal basal renal function already have reduced (Group A) renal functional reserve capacity, which is completely abolished (Group B) when concomitant hyperfiltration occurs. ACE inhibition reduces hyperfiltration and is capable of blocking the AA-induced rise in GFR in these patients.
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PMID:[Behavior of the renal functional reserve in type I diabetic patients: effect of ACE-inhibition]. 221

Our results as well as those in the literature suggest that some hormone or combination of hormones, that are inhibited by somatostatin, is responsible for the hyperfiltration response following amino acid infusion/protein ingestion. Recently, we have infused amino acids with somatostatin and replaced the stimulated levels of insulin/glucagon/growth hormone observed during amino acid infusion alone (Castellino and DeFronzo, preliminary results). This combined hormone replacement was able to overcome the inhibitory effect of somatostatin and return the increase in RPF and GFR to the elevated levels observed following amino acid infusion. These results suggest that some combination of these hormones is involved in the hyperfiltration response to hyperaminoacidemia. However, several comments are worthy of emphasis. First, somatostatin is known to inhibit a number of hormones (Table 1), and a contributory role for any of these should not be excluded. Second, a large body of evidence has accumulated to indicate that neither insulin, glucagon, nor growth hormone alone are capable of augmenting either RPF or GFR. The possibility that infusion of the three hormones together will increase RPF and GFR, when neither hormone alone will do so, has not been examined. More likely, some interaction between the elevated plasma amino acid concentrations and the elevated hormone levels is responsible for the hyperfiltration response. It is interesting to speculate that such an interaction might be exerted at the level of the kidney by an effect on renal amino acid metabolism.
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PMID:Regulation of renal hemodynamics by plasma amino acid and hormone concentrations. 332 9


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