Cited by 59Ion Transport and Channel RegulationChronic Kidney Disease and DiabetesPancreatic function and diabetes

Influence of glucagon on GFR and on urea and electrolyte excretion: direct and indirect effects

Ahloulay, M., Dechaux, M., Laborde, K., Bankir, L.·1995·American Journal of Physiology-Renal Physiology

Abstract

Clearance experiments were performed in anesthetized male Wistar rats to determine the level of peripheral glucagon concentration required to elicit changes in glomerular filtration rate (GFR) and in solute excretion. Glucagon was intravenously infused at a rate of 1.25 (group G-1, n = 8), 3.75 (group G-3, n = 7), or 12.5 (group G-10, n = 7) ng.min-1.100 g body wt-1 for 100 min. Measurements were performed before, during, and after this infusion. Group G-10 resulted in a plasma concentration of glucagon severalfold higher than usually observed in peripheral blood after a protein meal but normal for the hepatic circulation. Group G-10 simultaneously increased GFR, plasma adenosine 3',5'-cyclic monophosphate (cAMP) concentration, and the excretion of water (i.e., urinary flow rate), Na, Cl, PO4, K, and urea. Some of the effects of glucagon on electrolyte excretion were also observed with group G-1 and/or G-3 and were fully reversible, suggesting a direct renal action of glucagon. The significant and reversible increase in K excretion in group G-3 suggests that glucagon exerts a direct stimulatory influence on K secretion in the distal nephron. Increases in urinary flow rate, PO4, Na, and urea fractional excretions were seen with group G-10 only and were not reversible, suggesting an indirect action of glucagon on the proximal tubule. Because glucagon stimulates cAMP formation in hepatocytes and because this cAMP is released in the blood and secreted by proximal tubule cells, cAMP of hepatic origin could induce a parathyroid hormone-like effect in this nephron segment. In summary, these experiments suggest that glucagon influences different aspects of renal function by a combination of direct and indirect (probably liver-dependent) effects.

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Crossref · 10.1152/ajprenal.1995.269.2.f225

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Authors
Ahloulay, M., Dechaux, M., Laborde, K., & Bankir, L.
Affiliations
  • Hôpital Necker-Enfants Malades (FR)
  • Institut National de la Sante et de la Recherche Medicale Unite 90,Hopital Necker-Enfants Malades, Paris, France.
Venue
American Journal of Physiology-Renal Physiology
Published
1995-08-01
Volume
269
Issue
2
Pages
F225-F235
ISSN
  • 1522-1466 (ISSN-L)
  • 1931-857X
OpenAlex
W2337023143
Cited by
59
References
0
Citations by year
2026: 1 · 2025: 3 · 2024: 3 · 2023: 1 · 2021: 3 · 2020: 2 · 2019: 1 · 2018: 3 · 2017: 1 · 2016: 2 · 2015: 3 · 2014: 3 · 2012: 3
FWCI
0.61
Type
journal article
Language
en
Open access
closed
Locations
  • American Journal of Physiology-Renal Physiology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Ion Transport and Channel Regulation
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
Keywords
glucagon, glomerular filtration rate, renal electrolyte excretion, urea excretion, cyclic AMP, potassium secretion, distal nephron, proximal tubule
MeSH terms
Cyclic AMP, Animals, Diuresis, Electrolytes, Glomerular Filtration Rate, Glucagon, Male, Plasma, Urea, Urine, Rats, Wistar, Rats

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