The circadian clock modulates renal sodium handling.

Détails

Ressource 1Télécharger: BIB_4E9C79612EC0.P001.pdf (1872.06 [Ko])
Etat: Public
Version: Author's accepted manuscript
ID Serval
serval:BIB_4E9C79612EC0
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
The circadian clock modulates renal sodium handling.
Périodique
Journal of the American Society of Nephrology
Auteur(s)
Nikolaeva S., Pradervand S., Centeno G., Zavadova V., Tokonami N., Maillard M., Bonny O., Firsov D.
ISSN
1533-3450 (Electronic)
ISSN-L
1046-6673
Statut éditorial
Publié
Date de publication
2012
Peer-reviewed
Oui
Volume
23
Numéro
6
Pages
1019-1026
Langue
anglais
Notes
Publication types: Comparative Study ; Journal Article ; Research Support, Non-U.S. Gov'tPublication
Résumé
The circadian clock contributes to the control of BP, but the underlying mechanisms remain unclear. We analyzed circadian rhythms in kidneys of wild-type mice and mice lacking the circadian transcriptional activator clock gene. Mice deficient in clock exhibited dramatic changes in the circadian rhythm of renal sodium excretion. In parallel, these mice lost the normal circadian rhythm of plasma aldosterone levels. Analysis of renal circadian transcriptomes demonstrated changes in multiple mechanisms involved in maintaining sodium balance. Pathway analysis revealed the strongest effect on the enzymatic system involved in the formation of 20-HETE, a powerful regulator of renal sodium excretion, renal vascular tone, and BP. This correlated with a significant decrease in the renal and urinary content of 20-HETE in clock-deficient mice. In summary, this study demonstrates that the circadian clock modulates renal function and identifies the 20-HETE synthesis pathway as one of its principal renal targets. It also suggests that the circadian clock affects BP, at least in part, by exerting dynamic control over renal sodium handling.
Mots-clé
Aldosterone/analysis, Aldosterone/blood, Animals, CLOCK Proteins/genetics, CLOCK Proteins/metabolism, Circadian Clocks/genetics, Disease Models, Animal, Homeostasis/genetics, Hydroxyeicosatetraenoic Acids/metabolism, Kidney Concentrating Ability, Kidney Tubules, Collecting/metabolism, Linear Models, Mice, Mice, Inbred C57BL, Mice, Knockout, Random Allocation, Renin-Angiotensin System/physiology, Sensitivity and Specificity, Sodium/metabolism, Sodium/urine, Transcriptome/genetics
Pubmed
Web of science
Open Access
Oui
Création de la notice
29/11/2012 19:17
Dernière modification de la notice
20/10/2020 11:12
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