Lack of Renal Tubular Glucocorticoid Receptor Decreases the Thiazide-Sensitive Na<sup>+</sup>/Cl<sup>-</sup> Cotransporter NCC and Transiently Affects Sodium Handling.

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Etat: Public
Version: de l'auteur
Licence: CC BY 4.0
ID Serval
serval:BIB_8E551F087D5A
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Lack of Renal Tubular Glucocorticoid Receptor Decreases the Thiazide-Sensitive Na<sup>+</sup>/Cl<sup>-</sup> Cotransporter NCC and Transiently Affects Sodium Handling.
Périodique
Frontiers in physiology
Auteur(s)
Canonica J., Frateschi S., Boscardin E., Ebering A., Sergi C., Jäger Y., Peyrollaz T., Mérillat A.M., Maillard M., Klusonova P., Odermatt A., Koesters R., Debonneville A., Staub O., Verouti S.N., Hummler E.
ISSN
1664-042X (Print)
ISSN-L
1664-042X
Statut éditorial
Publié
Date de publication
2019
Peer-reviewed
Oui
Volume
10
Pages
989
Langue
anglais
Notes
Publication types: Journal Article
Publication Status: epublish
Résumé
Chronic glucocorticoid infusion impairs NCC activity and induces a non-dipping profile in mice, suggesting that glucocorticoids are essential for daily blood pressure variations. In this paper, we studied mice lacking the renal tubular glucocorticoid receptor (GR) in adulthood (GR knockouts, Nr3c1 <sup>
Pax8/LC1
</sup> ). Upon standard salt diet, Nr3c1 <sup>
Pax8/LC1
</sup> mice grow normally, but show reduced NCC activity despite normal plasma aldosterone levels. Following diet switch to low sodium, Nr3c1 <sup>
Pax8/LC1
</sup> mice exhibit a transient but significant reduction in the activity of NCC and expression of NHE3 and NKCC2 accompanied by significant increased Spak activity. This is followed by transiently increased urinary sodium excretion and higher plasma aldosterone concentrations. Plasma corticosterone levels and 11βHSD2 mRNA expression and activity in the whole kidney remain unchanged. High salt diet does not affect whole body Na <sup>+</sup> and/or K <sup>+</sup> balance and NCC activity is not reduced, but leads to a significant increase in diastolic blood pressure dipping in Nr3c1 <sup>
Pax8/LC1
</sup> mice. When high sodium treatment is followed by 48 h of darkness, NCC abundance is reduced in knockout mice although activity is not different. Our data show that upon Na <sup>+</sup> restriction renal tubular GR-deficiency transiently affects Na <sup>+</sup> handling and transport pathways. Overall, upon standard, low Na <sup>+</sup> and high Na <sup>+</sup> diet exposure Na <sup>+</sup> and K <sup>+</sup> balance is maintained as evidenced by normal plasma and urinary Na <sup>+</sup> and K <sup>+</sup> and aldosterone concentrations.
Mots-clé
Na+-K+-Cl– cotransporter, blood pressure, blood pressure dipping, glucocorticoid receptor, sodium and hydrogen exchanger 3, sodium transport, thiazide-sensitive Na+/Cl– cotransporter
Pubmed
Web of science
Open Access
Oui
Création de la notice
13/09/2019 17:51
Dernière modification de la notice
22/01/2020 6:26
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