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Cited by 136Chronic Kidney Disease and DiabetesRenin-Angiotensin System StudiesRenal Diseases and Glomerulopathies

Vasopressin increases urinary albumin excretion in rats and humans: involvement of V2 receptors and the renin-angiotensin system

Bardoux, P.·2003·Nephrology Dialysis Transplantation
DOI 10.1093/ndt/18.3.497
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Abstract

BACKGROUND: An increase in urinary albumin excretion (UAE) represents an early predictor of glomerular damage in diabetes mellitus (DM) and a risk factor for cardiovascular complications in hypertension. Vasopressin is elevated in DM and in some forms of hypertension. Previous studies in rats suggested that this hormone could play a role in the albuminuria observed in chronic renal failure or diabetic nephropathy, but no information is available concerning the mechanism of these effects and the possible influence of vasopressin on UAE in the healthy kidney. The present study was thus designed to evaluate whether vasopressin influences UAE in normal rats and humans, whether this effect is V(2)-receptor-dependent, and whether it is mediated by the renin-angiotensin system. METHODS: UAE was measured in normal Wistar rats and healthy humans, or in subjects with various forms of diabetes insipidus (DI), before and after acute or chronic infusion of the vasopressin V(2) receptor agonist dDAVP. Chronic dDAVP administration was also performed in normal Wistar rats previously submitted to either chronic angiotensin-converting enzyme inhibition (ACEI) or chronic blockade of AT1 receptors (ARB). RESULTS: In rats, acute or chronic dDAVP infusion increased UAE significantly and reversibly (4-fold and 6-fold, respectively). In healthy subjects, acute infusion of dDAVP tripled UAE (P<0.01) but did not change creatinine and beta(2)-microglobulin excretion, thus suggesting that the rise in UAE was due to an increased glomerular leakage of albumin. dDAVP also increased UAE in patients with central DI and in patients with hereditary nephrogenic DI bearing AQP2 mutations. However, UAE was not increased in patients with hereditary nephrogenic DI bearing mutations of the V(2) receptor. In rats, ACEI and ARB blunted the dDAVP-induced rise in UAE by 70% (P<0.05) and 50% (NS), respectively. CONCLUSIONS: The present studies reveal for the first time that vasopressin induces a marked increase in UAE in healthy rats and humans. This albuminuric effect seems to result from increased glomerular leakage, requires functional vasopressin V(2) receptors, and is, at least in part, mediated by the renin-angiotensin system. These results bring additional support for an involvement of vasopressin in the albuminuria observed in pathological states such as diabetes mellitus or hypertension.

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Authors
Bardoux, P.
Affiliations
Inserm (FR)
Corresponding author
Bardoux, P.
Venue
Nephrology Dialysis Transplantation
Publisher
Oxford University Press (OUP)
Published
2003-03-01
Volume
18
Issue
3
Pages
497-506
ISSN
  • 0931-0509 (ISSN-L)
  • 1460-2385
DOI
10.1093/ndt/18.3.497
OpenAlex
W2120793874
Cited by
136
References
23
Citations by year
2024: 7 · 2023: 6 · 2022: 5 · 2021: 6 · 2020: 7 · 2019: 11 · 2018: 9 · 2017: 12 · 2016: 8 · 2015: 10 · 2014: 9 · 2013: 7 · 2012: 3
FWCI
1.50
Type
journal article
Language
en
Open access
closed
Locations
  • Nephrology Dialysis Transplantation (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Renin-Angiotensin System Studies
  • Health Sciences › Medicine › Nephrology › Renal Diseases and Glomerulopathies
Keywords
urinary albumin excretion, albuminuria, V2 receptor, renin-angiotensin system, desmopressin, diabetes insipidus, nephrogenic diabetes insipidus, angiotensin-converting enzyme inhibition, AT1 receptor blockade, diabetes mellitus
MeSH terms
Adult, Albuminuria, Animals, Blood Pressure, Deamino Arginine Vasopressin, Diabetes Insipidus, Female, Humans, Male, Reference Values, Renal Agents, Renin-Angiotensin System, Vasopressins, Receptors, Vasopressin, Rats

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