Evidence map›Paper›PMID 23171553›Full record

ArticleAmerican journal of physiology. Renal physiology2013

Feedback inhibition of ENaC during acute sodium loading in vivo.

Ankit B Patel, Gustavo Frindt, Lawrence G Palmer

Abstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. ENaC processing in rat kidney: effects of salt loading and ADH.American journal of physiology. Renal physiology · 2026
    Article
  2. Article
  3. Control of ENaC ubiquitination.American journal of physiology. Renal physiology · 2024
    Article
  4. Influence of proteolytic cleavage of ENaC's γ subunit upon NaAmerican journal of physiology. Renal physiology · 2024
    Article
  5. Article
  6. Review
  7. Deletion of Kir5.1 abolishes the effect of high NaAmerican journal of physiology. Renal physiology · 2021
    Article
  8. Article
  9. Article
  10. Maintaining KAmerican journal of physiology. Renal physiology · 2016
    Review
  11. Brakes and gas-regulation of ENaC by sodium.Channels (Austin, Tex.) · 2016
    Article
  12. Article
  13. Intracellular Na+ regulates epithelial Na+ channel maturation.The Journal of biological chemistry · 2015
    Article
  14. Review
  15. The role of ENaC in vascular endothelium.Pflugers Archiv : European journal of physiology · 2014
    Review
  16. Review
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

3 authors at 1 institution in 1 country.

Ankit B PatelDepartment of Physiology and Biophysics, Weill Cornell Medical College, New York, NY 10065, USA.
Gustavo Frindt
Lawrence G Palmer
Cornell University · US

Funding

Weill Cornell/Rockefeller/Sloan-Kettering MST ProgramT32GM007739 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI HSU, KATHARINE C · 1985 to 2023
$51.1M
Epithelial Na Channels and Regulation of Na ExcretionR01DK059659 · NIDDK · WEILL MEDICAL COLL OF CORNELL UNIV · PI PALMER, LAWRENCE G · 2002 to 2012
$3.7M
NIDDK NIH HHS R01-DK-59659NIGMS NIH HHS GM-07739NIGMS NIH HHS T32 GM007739
6 · The paper itself

Abstract

The epithelial Na(+) channel (ENaC) is tightly regulated by sodium intake to maintain whole body sodium homeostasis. In addition, ENaC is inhibited by high levels of intracellular Na(+) [Na(+)](i), presumably to prevent cell Na(+) overload and swelling. However, it is not clear if this regulation is relevant in vivo. We show here that in rats, an acute (4 h) oral sodium load decreases whole-cell amiloride-sensitive currents (I(Na)) in the cortical collecting duct (CCD) even when plasma aldosterone levels are maintained high by infusing the hormone. This was accompanied by decreases in whole-kidney cleaved α-ENaC (2.6 fold), total β-ENaC (1.7 fold), and cleaved γ-ENaC (6.2 fold). In addition, cell-surface β- and γ-ENaC expression was measured using in situ biotinylation. There was a decrease in cell-surface core-glycosylated (2.2 fold) and maturely glycosylated (4.9 fold) β-ENaC and cleaved γ-ENaC (4.7 fold). There were no significant changes for other apical sodium transporters. To investigate the role of increases in Na(+) entry and presumably [Na(+)](i) on ENaC, animals were infused with amiloride prior to and during sodium loading. Blocking Na(+) entry did not inhibit the effect of resalting on I(Na). However, amiloride did prevent decreases in ENaC expression, an effect that was not mimicked by hydrochlorothiazide administration. Na(+) entry and presumably [Na(+)](i) can regulate ENaC expression but does not fully account for the aldosterone-independent decrease in I(Na) during an acute sodium load.

Indexed as

AldosteroneAmilorideAnimalsDiureticsEpithelial Sodium ChannelsFeedback, PhysiologicalFemaleGene Expression RegulationRatsRats, Sprague-DawleySodiumSpecific Pathogen-Free OrganismsWaterWater-Electrolyte BalanceAldosteroneAmilorideDiureticsEpithelial Sodium ChannelsSodiumWater

Identifiers

PMID23171553
PMCPMC3543624
OpenAlexW2158164926

What OpenQuestion holds

Textmetadata
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.