ENaC activity in collecting ducts modulates NCC in cirrhotic mice.

Détails

Ressource 1Télécharger: 5_26055235_Postprint.pdf (5867.81 [Ko])
Etat: Serval
Version: Author's accepted manuscript
ID Serval
serval:BIB_EEAFFA21DE0F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
ENaC activity in collecting ducts modulates NCC in cirrhotic mice.
Périodique
Pflügers Archiv : European Journal of Physiology
Auteur(s)
Mordasini D., Loffing-Cueni D., Loffing J., Beatrice R., Maillard M.P., Hummler E., Burnier M., Escher G., Vogt B.
ISSN
1432-2013 (Electronic)
ISSN-L
0031-6768
Statut éditorial
Publié
Date de publication
2015
Peer-reviewed
Oui
Volume
467
Numéro
12
Pages
2529-2539
Langue
anglais
Notes
Publication types: Journal Article ; Research Support, Non-U.S. Gov't
Publication Status: ppublish
Résumé
Cirrhosis is a frequent and severe disease, complicated by renal sodium retention leading to ascites and oedema. A better understanding of the complex mechanisms responsible for renal sodium handling could improve clinical management of sodium retention. Our aim was to determine the importance of the amiloride-sensitive epithelial sodium channel (ENaC) in collecting ducts in compensate and decompensate cirrhosis. Bile duct ligation was performed in control mice (CTL) and collecting duct-specific αENaC knockout (KO) mice, and ascites development, aldosterone plasma concentration, urinary sodium/potassium ratio and sodium transporter expression were compared. Disruption of ENaC in collecting ducts (CDs) did not alter ascites development, urinary sodium/potassium ratio, plasma aldosterone concentrations or Na,K-ATPase abundance in CCDs. Total αENaC abundance in whole kidney increased in cirrhotic mice of both genotypes and cleaved forms of α and γ ENaC increased only in ascitic mice of both genotypes. The sodium chloride cotransporter (NCC) abundance was lower in non-ascitic KO, compared to non-ascitic CTL, and increased when ascites appeared. In ascitic mice, the lack of αENaC in CDs induced an upregulation of total ENaC and NCC and correlated with the cleavage of ENaC subunits. This revealed compensatory mechanisms which could also take place when treating the patients with diuretics. These compensatory mechanisms should be considered for future development of therapeutic strategies.
Mots-clé
Aldosterone/blood, Animals, Bile Ducts/metabolism, Epithelial Sodium Channels/genetics, Epithelial Sodium Channels/metabolism, Liver Cirrhosis, Experimental/metabolism, Mice, Potassium/urine, Sodium/urine, Sodium Chloride Symporters/metabolism
Pubmed
Web of science
Création de la notice
07/10/2015 17:33
Dernière modification de la notice
03/03/2018 22:33
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