Feedback inhibition of rat amiloride-sensitive epithelial sodium channels expressed in Xenopus laevis oocytes.

Détails

ID Serval
serval:BIB_A1AE70F4D2D3
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Feedback inhibition of rat amiloride-sensitive epithelial sodium channels expressed in Xenopus laevis oocytes.
Périodique
Journal of Physiology
Auteur(s)
Abriel H., Horisberger J.D.
ISSN
0022-3751
Statut éditorial
Publié
Date de publication
1999
Peer-reviewed
Oui
Volume
516
Numéro
Pt 1
Pages
31-43
Langue
anglais
Résumé
1. Regulation of the amiloride-sensitive epithelial sodium channel (ENaC) is essential for the control of body sodium homeostasis. The downregulation of the activity of this Na+ channel that occurs when the intracellular Na+ concentration ([Na+]i) is increased is known as feedback inhibition. Although intracellular Na+ is the trigger for this phenomenon, its cellular and molecular mediators are unknown. 2. We used the 'cut-open oocyte' technique to control the composition of the intracellular milieu of Xenopus oocytes expressing rat ENaCs to enable us to test several factors potentially involved in feedback inhibition. 3. The effects of perfusion of the intracellular space were demonstrated by an electromicrographic study and the time course of the intracellular solution exchange was established by observing the effect of intracellular pH: a decrease from pH 7.4 to 6.5 reduced the amiloride-sensitive current by about 40 % within 2 min. 4. Feedback inhibition was observed in non-perfused oocytes when Na+ entry induced a large increase in [Na+]i. Intracellular perfusion prevented feedback regulation even though the [Na+]i was allowed to increase to values above 50 mM. 5. No effects on the amiloride-sensitive current were observed after changes in the concentration of Na+ (from 1 to 50 mM), Ca2+ (from 10 to 1000 nM) or ATP (from nominally free to 1 or 5 mM) in the intracellular perfusate. 6. We conclude that feedback inhibition requires intracellular factors that can be removed by intracellular perfusion. Although a rise in [Na+]i may be the trigger for the feedback inhibition of the ENaC, this effect is not mediated by a direct effect of Na+, Ca2+ or ATP on the ENaC protein.
Mots-clé
Adenosine Triphosphate, Amiloride, Animals, Calcium, Cell Membrane, Diuretics, Down-Regulation, Epithelial Sodium Channel, Epithelium, Feedback, Female, Kinetics, Microscopy, Electron, Oocytes, Patch-Clamp Techniques, Rats, Sodium, Sodium Channels, Xenopus laevis
Pubmed
Web of science
Open Access
Oui
Création de la notice
24/01/2008 11:56
Dernière modification de la notice
08/05/2019 22:59
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