Effect of glycine and glucagon on glomerular filtration and renal metabolic rates

Johannesen, Justin; Lie, Mons; Kiil, Fredrik

doi:10.1152/ajprenal.1977.233.1.f61

Cited by 35 publications

(26 citation statements)

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“…was increased by GLN in Experiment 2, the filtration fraction increased at the higher GLN dosages. This is consistent with results from other studies utilizing anaesthetized dogs (Staub, Springs, Stoll & Elrick, 1957;Pullman, Lavender & Aho, 1967;Stowe & Hook, 1970;Levy & Starr, 1972;Johannesen, Lie & Kiil, 1977) and indicates that sodium pentobarbitone anaesthesia alters renal vascular responsiveness. Therefore, effects in conscious and anaesthetized dogs may not be comparable.…”

Section: Discussionsupporting

confidence: 92%

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Glucagon and Alanine‐induced Increases of the Canine Renal Glomerular Filtration Rate

Palmore

1983

Exp Physiol

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Renal responses to intravenous DL‐alanine (ala) and glucagon (GLN) infusions were compared in conscious dogs. Doses of GLN (0·1 µg/min) that did not increase plasma glucose (PG) concentrations, a physiological effect of GLN, stimulated glomerular filtration rate (G.F.R.). Higher GLN infusion rates (1·0 and 10·0 µg/min) stimulated G.F.R., renal plasma flow (R.P.F.), PG, and potassium and urea clearances. Ala infusions (1·3 mmol/min) had similar effects if the dogs had been pre‐conditioned by feeding of corn starch, but not if they had been fed a normal diet. This level of ala infusion increased plasma a amino nitrogen to levels equivalent to plasma ala levels reported to stimulate GLN secretion. The reason for the lack of responsiveness to ala infusion when the normal diet was fed was not clear. When somatostatin (3·8, µg/min), an inhibitor of GLN secretion, and ala were infused simultaneously, G.F.R. was lower than when ala alone was infused. The data suggested that the ala‐induced renal effects were mediated by GLN.

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Section: Discussionsupporting

confidence: 92%

“…Several studies show that GLN increases electrolyte clearances (Staub et al 1957;Pullman et al 1967;Stowe & Hook, 1970;Levy & Starr, 1972;Johannesen et al: 1977). Unfortunately, the effects of GLN and ala in the present study on those clearances were distorted by the simultaneous saline infusions.…”

Section: Discussioncontrasting

confidence: 69%

Glucagon and Alanine‐induced Increases of the Canine Renal Glomerular Filtration Rate

Palmore

1983

Exp Physiol

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“…The hypothesis of ADH hyposecretion by PCS rats is supported by the fact that homozygous rats with hereditary diabetes in sipidus also manifest dramatic polyuria and excrete 80% less prostaglandins than con trols [12]. On the other hand, we have found plasma glucagon levels 3 times greater in PCS than in control rats [ 13], agreeing with other authors [14], Among the actions of this hormone an increase in glomerular filtration rate and diuresis can be included [15]. Thus, hyperglucagonemia of PCS rats may contrib ute to the aforementioned renal function de rangements.…”

Section: Discussionsupporting

confidence: 91%

Renal Function Derangements Induced by Portacaval Anastomosis in Normal Rats

Romeo

López‐Farré²,

Martín‐Paredero³

et al. 1991

Eur Surg Res

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The purpose of this study was to determine the renal function derangements that portacaval shunting caused in previously normal rats. Eight rats suffered a surgical portacaval shunt (PCS) and another 8 a sham operation (SHAM). Renal function was investigated by determining urinary volume, sodium, potassium, creatinine and aldosterone excretion, in basal conditions and after sodium overload. Plasma renin concentration and urinary excretion of PGE₂, 6-keto-PGF_1α and TXB₂ were also determined in basal conditions. PCS rats showed increased urinary volume, creatinine excretion and endogenous creatinine clearance, either in basal conditions or after sodium load. After the latter, PCS animals also showed sodium retention and hyperaldosteronuria. PCS caused in basal conditions a striking diminution in urinary excretion of all prostaglandins and no changes in plasma renin. In conclusion, PCS in the normal rat caused a renal dysfunction consisting of polyuria, possibly related to ADH disfunction and an inability to manage a sodium load.

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“…Infusion of octreotide to IDDM patients induced an acute reduction in RPF and GFR, and in addition plasma GH et al: Octreotide treatment of manifest diabetic renal changes and glucagon were decreased. The fall in glucagon concentration correlated significantly with the reduction in RPF and GFR [39], which is an interesting observation since glucagon may be involved in the diabetic renal hypertrophy-hyperfunction syndrome [40][41][42], though no conclusive results have been obtained [43]. In a long-term study octreotide administration for 12 weeks in IDDM patients caused a significant decrease in the elevated GFR, and total kidney volume was reduced as well.…”

Section: Discussionmentioning

confidence: 99%

Effect of octreotide and insulin on manifest renal and glomerular hypertrophy and urinary albumin excretion in long-term experimental diabetes in rats

et al. 1995

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Summary Treatment of diabetic rats with octreotide can inhibit early diabetic renal hypertrophy. Octreotide administration for 6 months from the day of diabetes induction inhibits renal hypertrophy and diminishes increase in urinary albumin excretion. To investigate the effect of octreotide on manifest diabetic renal changes, octreotide treatment was given for 3 weeks after an untreated diabetic period of 3 or 6 months. In addition, following 6 months of diabetes, a group of diabetic rats was treated with insulin for 3 weeks. Renal and glomerular hypertrophy, and increased urinary albumin excretion were observed in diabetic rats compared to non-diabetic control rats from 3 months and throughout the study period. Octreotide treatment did not affect body weight, food intake, blood glucose or serum fructosamine levels. We observed no effect of octreotide treatment on renal and glomerular hypertrophy or urinary albumin excretion compared to placebotreated diabetic rats. Insulin treatment for 3 weeks after 6 months of untreated diabetes normalized blood glucose and serum fructosamine levels, and furthermore renal hypertrophy was significantly diminished compared to the placebo-treated diabetic rats. However, insulin treatment had no effect on glomerular hypertrophy or urinary albumin excretion. In conclusion, octreotide treatment for 3 weeks following an untreated diabetic period of 3 or 6 months is unable to reduce the increased renal and glomerular volume or urinary albumin excretion. However, insulin treatment for 3 weeks with induction of euglycaemia diminishes the renal hypertrophy but has no effect on glomerular volume or urinary albumin excretion. [Diabetologia (1995) 38: 135-144]

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Effect of glycine and glucagon on glomerular filtration and renal metabolic rates

Cited by 35 publications

References 0 publications

Glucagon and Alanine‐induced Increases of the Canine Renal Glomerular Filtration Rate

Glucagon and Alanine‐induced Increases of the Canine Renal Glomerular Filtration Rate

Renal Function Derangements Induced by Portacaval Anastomosis in Normal Rats

Effect of octreotide and insulin on manifest renal and glomerular hypertrophy and urinary albumin excretion in long-term experimental diabetes in rats

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