Evidence map›Paper›PMID 25966345›Full record

ReviewSeminars in nephrology2015

Endothelin and renal ion and water transport.

Joshua S Speed, Brandon M Fox, Jermaine G Johnston, David M Pollock

Open access · greenAbstract readReview
In one paragraph

Review in Seminars in nephrology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

22 citing papers in PubMed, 40 citations in OpenAlex.

  1. Trial
  2. Salt and chronic kidney disease.Nature reviews. Nephrology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Oral administration of a dual ETMolecular vision · 2022
    Article
  10. Review
  11. Article
  12. High salt intake induces collecting duct HDAC1-dependent NO signaling.American journal of physiology. Renal physiology · 2021
    Article
  13. Article
  14. Role of GRK4 in the regulation of the renal ETB receptor in hypertension.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  15. Article
  16. Circadian regulation of kidney function: finding a role for Bmal1.American journal of physiology. Renal physiology · 2018
    Review
  17. Circadian regulation of renal function.Free radical biology & medicine · 2018
    Review
  18. Article
  19. Article
  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

4 authors at 1 institution in 1 country.

Joshua S SpeedCardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Brandon M FoxCardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
Jermaine G JohnstonCardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL.
David M PollockCardio-Renal Physiology and Medicine, Division of Nephrology, Department of Medicine, University of Alabama at Birmingham, Birmingham, AL. Electronic address: dpollock@uab.edu.
University of Alabama at Birmingham · US

Funding

Vascular and renal responses to stressP01HL069999 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI HARSHFIELD, GREGORY ALAN · 2002 to 2018
$31.1M
UAB-UCSD O'Brien Core Center for Acute Kidney Injury ResearchP30DK079337 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI AGARWAL, ANUPAM · 2008 to 2022
$18.3M
Renal endothelin receptor-specific function in angiotensin ll-dependent hypertensP01HL095499 · NHLBI · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI POLLOCK, DAVID M · 2010 to 2014
$11.1M
The Role of Endothelin-1 in Sickle Cell DiseaseU01HL117684 · NHLBI · AUGUSTA UNIVERSITY · PI KUTLAR, ABDULLAH, MEILER, STEFFEN · 2013 to 2017
$8.1M
TRAINING IN CELLULAR PHYSIOLOGY MEMBRANE TRANSPORTT32DK007545 · NIDDK · UNIVERSITY OF ALABAMA AT BIRMINGHAM · PI GUTIERREZ, ORLANDO M · 1987 to 2023
$4.5M
NHLBI NIH HHS P01 HL069999NHLBI NIH HHS P01HL069999NHLBI NIH HHS P01 HL095499NHLBI NIH HHS P01HL095499NHLBI NIH HHS U01 HL117684NHLBI NIH HHS U01HL117684NIDDK NIH HHS T32 DK007545NIDDK NIH HHS T32DK079337
6 · The paper itself

Abstract

The renal tubular epithelial cells produce more endothelin-1 (ET-1) than any other cell type in the body. Moving down the nephron, the amount of ET-1 produced appears fairly consistent until reaching the inner medullary collecting duct, which produces at least 10 times more ET-1 than any other segment. ET-1 inhibits Na(+) transport in all parts of the nephron through activation of the ETB receptor, and, to a minor extent, the ETA receptor. These effects are most prominent in the collecting duct where ETB-receptor activation inhibits activity of the epithelial Na(+) channel. Effects in other parts of the nephron include inhibition of Na(+)/H(+) exchange in the proximal tubule and the Na(+), K(+), 2Cl(-) co-transporter in the thick ascending limb. In general, the renal epithelial ET-1 system is an integral part of the body's response to a high salt intake to maintain homeostasis and normal blood pressure. Loss of ETB-receptor function results in salt-sensitive hypertension. The role of renal ET-1 and how it affects Na(+) and water transport throughout the nephron is reviewed.

Indexed as

AquaporinsEndothelinsHomeostasisHumansIon TransportKidney Tubules, CollectingKidney Tubules, ProximalSignal TransductionSodium ChlorideAquaporinsEndothelinsSodium ChlorideEndothelinkidneysodium transport

Identifiers

PMID25966345
PMCPMC4499165
OpenAlexW1590768755

What OpenQuestion holds

Textmetadata
LicenceTDM
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.