Evidence map›Paper›PMID 10066920›Full record

ArticleThe Journal of physiology1999

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

H Abriel, J D Horisberger

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of physiology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.9field-weighted citation impact, top 15% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

31 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
  2. Control of ENaC ubiquitination.American journal of physiology. Renal physiology · 2024
    Article
  3. Elevated intracellular NaProceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  4. Regulation of ion transport from within ion transit pathways.The Journal of general physiology · 2020
    Review
  5. Article
  6. Iron is a substrate of theThe Journal of biological chemistry · 2017
    Article
  7. Review
  8. Article
  9. Intracellular Na+ regulates epithelial Na+ channel maturation.The Journal of biological chemistry · 2015
    Article
  10. Article
  11. The role of ENaC in vascular endothelium.Pflugers Archiv : European journal of physiology · 2014
    Review
  12. Review
  13. Article
  14. Article
  15. Redox artifacts in electrophysiological recordings.American journal of physiology. Cell physiology · 2013
    Article
  16. Feedback inhibition of ENaC during acute sodium loading in vivo.American journal of physiology. Renal physiology · 2013
    Article
  17. Article
  18. Extracellular chloride regulates the epithelial sodium channel.The Journal of biological chemistry · 2009
    Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

2 authors at 1 institution in 1 country.

H AbrielInstitute of Pharmacology and Toxicology, School of Medicine, University of Lausanne, Switzerland.
J D Horisberger
University of Lausanne · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Adenosine TriphosphateAmilorideAnimalsCalciumCell MembraneDiureticsDown-RegulationEpithelial Sodium ChannelsEpitheliumFeedbackFemaleKineticsMicroscopy, ElectronOocytesPatch-Clamp TechniquesRatsAdenosine TriphosphateAmilorideCalciumDiureticsEpithelial Sodium ChannelsSodiumSodium Channels

Identifiers

PMID10066920
PMCPMC2269211
OpenAlexW2037737642

What OpenQuestion holds

Texttitle and abstract
measurements read1
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.