Evidence map›Paper›PMID 27188842›Full record

ReviewJournal of the American Society of Nephrology : JASN2016

Coordinated Control of ENaC and Na+,K+-ATPase in Renal Collecting Duct.

Eric Feraille, Eva Dizin

Open access · bronzeAbstract readReview
In one paragraph

Review in Journal of the American Society of Nephrology : JASN, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Review
  6. The epithelial NaCell communication and signaling : CCS · 2024
    Article
  7. Article
  8. Review
  9. Article
  10. The Triad NaInternational journal of molecular sciences · 2023
    Article
  11. Review
  12. Review
  13. Inward rectifier potassium (Kir) channels in the retina: living our vision.American journal of physiology. Cell physiology · 2022
    Review
  14. Review
  15. Renal water transport in health and disease.Pflugers Archiv : European journal of physiology · 2022
    Review
  16. Article
  17. Article
  18. Article
  19. Review
  20. 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

2 authors at 1 institution in 1 country.

Eric FerailleDepartment of Cell Biology and Metabolism, University of Geneva, Geneva, Switzerland Eric.Feraille@unige.ch.
Eva DizinDepartment of Cell Biology and Metabolism, University of Geneva, Geneva, Switzerland.
University of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tubular reabsorption of filtered sodium is tightly controlled to maintain body volume homeostasis. The rate of sodium transport by collecting duct (CD) cells varies widely in response to dietary sodium intake, GFR, circulating hormones, neural signals, and local regulatory factors. Reabsorption of filtered sodium by CD cells occurs via a two-step process. First, luminal sodium crosses the apical plasma membrane along its electrochemical gradient through epithelial sodium channels (ENaC). Intracellular sodium is then actively extruded into the interstitial space by the Na(+),K(+)-ATPase located along the basolateral membrane. Mismatch between sodium entry and exit induces variations in sodium intracellular concentration and cell volume that must be maintained within narrow ranges for control of vital cell functions. Therefore, renal epithelial cells display highly coordinated apical and basolateral sodium transport rates. We review evidence from experiments conducted in vivo and in cultured cells that indicates aldosterone and vasopressin, the two major hormones regulating sodium reabsorption by CD, generate a coordinated stimulation of apical ENaC and basolateral Na(+),K(+)-ATPase. Moreover, we discuss evidence suggesting that variations in sodium entry per se induce a coordinated change in Na(+),K(+)-ATPase activity through the signaling of protein kinases such as protein kinase A and p38 mitogen-activated protein kinase.

Indexed as

Renal ReabsorptionAnimalsEpithelial Sodium ChannelsHumansIon TransportKidney Tubules, CollectingSodium-Potassium-Exchanging ATPaseEpithelial Sodium ChannelsSodium-Potassium-Exchanging ATPasealdosteronecollecting ductsENaCepithelial sodium channelNa transportp38 mitogen-activated protein kinase

Identifiers

PMID27188842
PMCPMC5004664
OpenAlexW2401570697

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.