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• W3025231638 abstract "Dans le nephron distal sensible a l'aldosterone, le recepteur aux mineralocorticoides (RM) et le recepteur aux glucocorticoids (RG) sont exprimes et peuvent etre lies et actives par l'aldosterone et le Cortisol, respectivement. La reabsorption renale de sodium est principalement controlee par le RM. Cependant, des modeles experimentaux in vitro et in vivo suggerent que le RG pourrait egalement jouer un role dans le transport renal du sodium. Afin d'etudier l'implication du RG et/ou du RM exprimes dans les cellules epitheliales adultes dans le transport renal du sodium, nous avons genere deux modeles de souris, dans lesquelles l'expression du RG (Nr3c1Pax8/LC1) ou du RM (Nr3c2Pax8/LC1) peut etre abolie de maniere inductible et cela specifiquement dans les tubules renaux.Les souris deficientes pour le gene du RM survivent mais developpent un phenotype severe de PHA-1, caracterise par un retard de croissance, une augmentation des niveaux urinaires de Na+, une diminution de la concentration du Na+ dans le plasma, une hyperkaliemie et une augmentation des niveaux d'aldosterone plasmatique. Ce phenotype empire et devient letal lorsque les souris sont nourries avec une diete deficiente en sodium. Les niveaux d'expression en proteine de NCC, de la forme phosphorylee de NCC et de aENaC sont diminues, alors que l'expression en ARN messager et en proteine du RG est augmentee. Une diete riche en Na+ et pauvre en K+ ne corrige pas la concentration elevee d'aldosterone dans le plasma pour la ramener a des niveaux conformes, mais est suffisante pour corriger la perte de poids et les niveaux anormaux des electrolytes dans le plasma et l'urine.--In the aldosterone-sensitive distal nephron, both the mineralocorticoid (MR) and the glucocorticoid (GR) receptor are expressed. They can be bound and activated by aldosterone and Cortisol, respectively. Renal Na+ reabsorption is mainly controlled by MR. However, in vitro and in vivo experimental models suggest that GR may play a role in renal Na+ transport. Therefore, to investigate the implication of MR and/or GR in adult epithelial cells in renal sodium transport, we generated inducible renal tubule- specific MR (Nr3c2Pax8/LC1) and GR (Nr3c1Pax8/LC1) knockout mice.MR-deficient mice survived but developed a severe PHA-1 phenotype with failure to thrive, higher urinary Na+, decreased plasma Na+ levels, hyperkalemia and higher levels of plasma aldosterone. This phenotype further worsened and became lethal under a sodium-deficient diet. NCC protein expression and its phosphorylated form, as well as aENaC protein level were downregulated, whereas the mRNA and protein expression of GR was increased. A diet rich in Na+and low in K+ did not normalize plasma aldosterone to control levels, but was sufficient to restore body weight, plasma and urinary electrolytes.Upon switch to a Na+-deficient diet, GR-mutant mice exhibited transient increased urinary Na+ and decreased K+ levels, with transitory higher plasma K+ concentration preceded by a significant increase in plasma aldosterone levels within the 12 hours following diet switch. We found no difference in urinary aldosterone levels, plasma Na+ concentration and plasma corticosterone levels. Moreover, NHE3, NKCC2, NCC" @default.
• W3025231638 created "2020-05-21" @default.
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• W3025231638 date "2015-01-01" @default.
• W3025231638 modified "2023-09-27" @default.
• W3025231638 title "The role of the renal mineralocorticoid versus the glucocorticoid receptor in renal sodium and potassium transport" @default.
• W3025231638 hasPublicationYear "2015" @default.
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