Evidence map›Paper›PMID 33486988›Full record

ReviewHypertension (Dallas, Tex. : 1979)2021

Epithelial Sodium Channel and Salt-Sensitive Hypertension.

Stephanie M Mutchler, Annet Kirabo, Thomas R Kleyman

Open access · bronzeAbstract readReview
In one paragraph

Review in Hypertension (Dallas, Tex. : 1979), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
73citing papers in PubMed, 1 pooled it
9.8field-weighted citation impact, top 1% 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

73 citing papers in PubMed, 1 synthesis or guideline pooled it, 122 citations in OpenAlex.

  1. Pooled it
  2. Review
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  8. Saliva-driven surface-engineeredBioactive materials · 2026
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13 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

Stephanie M MutchlerFrom the Department of Medicine (S.M.M., T.R.K.), University of Pittsburgh, PA.
Annet KiraboDivision of Clinical Pharmacology, Department of Medicine, and Department of Molecular Physiology and Biophysics Vanderbilt University, Nashville, TN (A.K.).
Thomas R KleymanFrom the Department of Medicine (S.M.M., T.R.K.), University of Pittsburgh, PA.
University of Pittsburgh · USVanderbilt University · US

Funding

Single Nephron and MetabolomicsP30DK079307 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2008 to 2022
$13.4M
T32 Research Training in Diabetes and EndocrinologyT32DK007052 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI ROBERT M O'DOHERTY · 1986 to 2026
$6.3M
ENaC regulation and its role in blood pressure homeostasisR01HL147818 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI Annet Kirabo, Thomas R Kleyman · 2019 to 2026
$4.6M
Renal and Epithelial Biology Training ProgramT32DK061296 · NIDDK · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KLEYMAN, THOMAS R · 2002 to 2022
$3.1M
Role of Salt, Isoketal-modified Proteins and Dendritic Cells in HypertensionK01HL130497 · NHLBI · VANDERBILT UNIVERSITY MEDICAL CENTER · PI KIRABO, ANNET · 2016 to 2020
$803k
NHLBI NIH HHS K01 HL130497NHLBI NIH HHS R01 HL147818NIDDK NIH HHS P30 DK079307NIDDK NIH HHS T32 DK007052NIDDK NIH HHS T32 DK061296
6 · The paper itself

Abstract

The development of high blood pressure is influenced by genetic and environmental factors, with high salt intake being a known environmental contributor. Humans display a spectrum of sodium-sensitivity, with some individuals displaying a significant blood pressure rise in response to increased sodium intake while others experience almost no change. These differences are, in part, attributable to genetic variation in pathways involved in sodium handling and excretion. ENaC (epithelial sodium channel) is one of the key transporters responsible for the reabsorption of sodium in the distal nephron. This channel has an important role in the regulation of extracellular fluid volume and consequently blood pressure. Herein, we review the role of ENaC in the development of salt-sensitive hypertension, and present mechanistic insights into the regulation of ENaC activity and how it may accelerate sodium-induced damage and dysfunction. We discuss the traditional role of ENaC in renal sodium reabsorption and review work addressing ENaC expression and function in the brain, vasculature, and immune cells, and how this has expanded the implications for its role in the initiation and progression of salt-sensitive hypertension.

Indexed as

AnimalsBlood PressureEpithelial Sodium ChannelsHumansHypertensionIon TransportKidneyModels, BiologicalNephronsSodium Chloride, DietaryEpithelial Sodium ChannelsSodium Chloride, Dietaryblood pressureendotheliumextracellular fluidnephronssmooth musclesodium

Identifiers

PMID33486988
PMCPMC7878349
OpenAlexW3125136917

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.