Effects of Glucagon on Renal Function in Man*

Elrick, Harold; Huffman, E.R.; Hlad, C. J.; Wiiipple, N.; Staub, Alfred; Smith, A. E.; Yearwood-Drayton, V.

doi:10.1210/jcem-18-8-813

Cited by 68 publications

(18 citation statements)

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“…Figure I demonstrates the changes in plasma glucagon and kidney function produced by the infusion of Elrick et al [3] showed that glucagon (0.9-7.5 trig) administered as a single dose intramuscularly or intravenously, or as a continuous intravenous infusion, increased GFR and RPF by approximately 10-15 per cent in normal man. Butturini et al [1] found an increase of about 10 per cent in GFR and RPF, giving a single intravenous injection of 1 to 3 mg glucagon in normal man.…”

Section: Resultsmentioning

confidence: 99%

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The effect of short-term glucagon infusion on kidney function in normal man

et al. 1977

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Summary. Kidney function was studied in six normal males before and during a 2 h glucagon (10ng/kg/min) infusion. The following variables were determined during each 20 min clearance period; glomerular filtration rate (GFR), renal plasma-flow (RPF), filtration fraction (FF), urinary albumin and/32-microglobulin-excretion rates. Glucagon infusion resulted in a fourfold increase in plasma glucagon concentration. The infusion induced a significant increase in GFR (+9%), FF (+ 9%) and urinary fl2-microglobulin excretion rate (+ 32%), (p < 0.01). RPF and urinary albumin excretion rates were not significantly changed. We suggest that glucagon may contribute to the reversible kidney function alterations typically found in poorly regulated juvenile diabetes, a state with relative or absolute hyperglucagonaemia.

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Section: Resultsmentioning

confidence: 99%

“…Enhanced GFR has been demonstrated in animals and man during glucagon infusion in pharmacological doses [1, 3,7]. Therefore, glucagon might be involved in the pathogenesis of the kidney function alterations in diabetes.…”

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The effect of short-term glucagon infusion on kidney function in normal man

et al. 1977

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“…Plasma glucagon concentration increases during fasting and decreases during refeeding (21,22). Since glucagon is known to have natriuretic properties (23)(24)(25)(26), sodium retention during refeeding could be related, at least in part, to a reduction in plasma glucagon concentration. However, carbohydrate-stimulated insulin secretion is also temporally related to sodium retention, and one may reasonably raise the question whether insulin plays a role in this phenomenon.…”

Section: Introductionmentioning

confidence: 99%

The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man.

DeFronzo¹,

Cooke²,

Andres³

et al. 1975

J. Clin. Invest.

1,032

418

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A B S T R A C T 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 PU/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±46 (SEM) to 213+18 iteq/min during insulin administration, the change becoming significant (P < 0.02) within the 30-60-min collection period. Free water clearance (CH2o) increased from 10.6±0.6 to 13±0.5 ml/min (P <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 (Ui.V) excretion were also both decreased during insulin administration; UKV decreased from 66±9 to 21±1 Meq/min (P < 0.005), and UrV decreased from 504±93 to 230 ±43 Ag/min (P <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±24 to 200±17 ug/min (P < 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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“…The observations reviewed in this paper show that cAMP should no longer be regarded only as an intracellular second messenger but also as a first messenger responsible for coordinated hepatorenal functions, and possibly for paracrine regulations in several other tissues. Dictyostelium discoideum; liver; adipose tissue; glucagon; epinephrine; parathyroid hormone; insulin; hypertension; hepatorenal syndrome; diabetes mellitus; sodium; phosphate GLUCAGON, A PANCREATIC HORMONE secreted after ingestion of proteins, has been known for a long time to be natriuretic and phosphaturic (56,66,105,142) and to increase renal blood flow and glomerular filtration rate …”

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Extracellular cAMP inhibits proximal reabsorption: are plasma membrane cAMP receptors involved?

Bankir

Ahloulay

Devreotes³

et al. 2002

American Journal of Physiology-Renal Physiology

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A.Parent. Extracellular cAMP inhibits proximal reabsorption: are plasma membrane cAMP receptors involved? Am J Physiol Renal Physiol 282: F376-F392, 2002; 10.1152/ajprenal.00202.2001.-Glucagon binding to hepatocytes has been known for a long time to not only stimulate intracellular cAMP accumulation but also, intriguingly, induce a significant release of liver-borne cAMP in the blood. Recent experiments have shown that the well-documented but ill-understood natriuretic and phosphaturic actions of glucagon are actually mediated by this extracellular cAMP, which inhibits the reabsorption of sodium and phosphate in the renal proximal tubule. The existence of this "pancreato-hepatorenal cascade" indicates that proximal tubular reabsorption is permanently influenced by extracellular cAMP, the concentration of which is most probably largely dependent on the insulinto-glucagon ratio. The possibility that renal cAMP receptors may be involved in this process is supported by the fact that cAMP has been shown to bind to brush-border membrane vesicles. In other cell types (i.e., adipocytes, erythrocytes, glial cells, cardiomyocytes), cAMP eggress and/or cAMP binding have also been shown to occur, suggesting additional paracrine effects of this nucleotide.Although not yet identified in mammals, cAMP receptors (cARs) are already well characterized in lower eukaryotes. The amoeba Dictyostelium discoideum expresses four different cARs during its development into a multicellular organism. cARs belong to the superfamily of seven transmembrane domain G protein-coupled receptors and exhibit a modest homology with the secretin receptor family (which includes PTH receptors). However, the existence of specific cAMP receptors in mammals remains to be demonstrated. Disturbances in the pancreato-hepatorenal cascade provide an adequate pathophysiological understanding of several unexplained observations, including the association of hyperinsulinemia and hypertension, the hepatorenal syndrome, and the hyperfiltration of diabetes mellitus. The observations reviewed in this paper show that cAMP should no longer be regarded only as an intracellular second messenger but also as a first messenger responsible for coordinated hepatorenal functions, and possibly for paracrine regulations in several other tissues. Dictyostelium discoideum; liver; adipose tissue; glucagon; epinephrine; parathyroid hormone; insulin; hypertension; hepatorenal syndrome; diabetes mellitus; sodium; phosphate GLUCAGON, A PANCREATIC HORMONE secreted after ingestion of proteins, has been known for a long time to be natriuretic and phosphaturic (56,66,105,142) and to increase renal blood flow and glomerular filtration rate

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Effects of Glucagon on Renal Function in Man*

Cited by 68 publications

References 0 publications

The effect of short-term glucagon infusion on kidney function in normal man

The effect of short-term glucagon infusion on kidney function in normal man

The effect of insulin on renal handling of sodium, potassium, calcium, and phosphate in man.

Extracellular cAMP inhibits proximal reabsorption: are plasma membrane cAMP receptors involved?

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