Sodium retention in rats with liver cirrhosis is associated with increased renal abundance of NaCl cotransporter (NCC)

Détails

ID Serval
serval:BIB_A8B64A1EED28
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Institution
Titre
Sodium retention in rats with liver cirrhosis is associated with increased renal abundance of NaCl cotransporter (NCC)
Périodique
Nephrology, Dialysis, Transplantation
Auteur(s)
Yu  Z., Serra  A., Sauter  D., Loffing  J., Ackermann  D., Frey  F. J., Frey  B. M., Vogt  B.
ISSN
0931-0509 (Print)
Statut éditorial
Publié
Date de publication
09/2005
Volume
20
Numéro
9
Pages
1833-41
Notes
Journal Article
Research Support, Non-U.S. Gov't --- Old month value: Sep
Résumé
BACKGROUND: Liver cirrhosis is associated with enhanced renal tubular sodium retention, the mechanism of which is still debated. We hypothesized that liver cirrhosis is associated with increased expression of renal epithelial sodium transporter(s). METHODS: Liver cirrhosis was induced by bile duct ligation (BDL) in rats. Steady state mRNA of ENaC subunits alpha, beta, gamma serum and glucocorticoid inducible kinase (Sgk1) were measured by TaqMan PCR in kidney homogenates at week 1, 2, 3 and 4 after BDL. Renal protein content of ENaC subunits, ubiquitin-protein-ligase Nedd4-2 and NaCl cotransporter (NCC) were assessed by western blot. Subcellular localization of ENaC subunits and NCC were analysed by immunohistochemistry. RESULTS: Steady state mRNA of ENaC alpha, beta and gamma were unchanged during the 4 weeks investigated, while ENaC protein decreased most prominently at week 2 (control vs BDL; alpha, -46%; beta, -81%; and gamma, -63%; n = 6). Subcellular localization of ENaC subunits was not altered at week 2. Sgk1 mRNA did not change, whereas Nedd4-2 protein was reduced by >50% 2-4 weeks after BDL. NCC protein significantly increased at week 1 (control vs BDL: +66%, n = 6, P<0.05) and decreased at week 3 (control vs BDL: -85%, n = 6, P<0.0005). CONCLUSIONS: Enhanced abundance of NCC was observed in the initial stage after BDL, followed by a marked decrease. ENaC transcription, translation or cell surface abundance was not increased after BDL.
Mots-clé
Aldosterone/blood Animals Bile Ducts/physiology Creatinine/blood Epithelial Sodium Channel Kidney/metabolism/*physiopathology Liver Cirrhosis, Experimental/*metabolism Male Polymerase Chain Reaction Potassium/urine Protein Subunits/genetics RNA, Messenger/genetics Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction Sodium/*metabolism/urine Sodium Channels/*genetics Sodium-Potassium-Chloride Symporters/*genetics/*metabolism
Pubmed
Web of science
Open Access
Oui
Création de la notice
25/01/2008 13:03
Dernière modification de la notice
20/08/2019 15:13
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