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

Details

Serval ID
serval:BIB_A1AE70F4D2D3
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Feedback inhibition of rat amiloride-sensitive epithelial sodium channels expressed in Xenopus laevis oocytes.
Journal
Journal of Physiology
Author(s)
Abriel H., Horisberger J.D.
ISSN
0022-3751
Publication state
Published
Issued date
1999
Peer-reviewed
Oui
Volume
516
Number
Pt 1
Pages
31-43
Language
english
Abstract
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.
Keywords
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
Yes
Create date
24/01/2008 10:56
Last modification date
20/08/2019 15:07
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