Evidence map›Paper›PMID 28003189›Full record

ReviewAmerican journal of physiology. Renal physiology2017

Involvement of ENaC in the development of salt-sensitive hypertension.

Tengis S Pavlov, Alexander Staruschenko

Open access · bronzeAbstract readReview
In one paragraph

Review in American journal of physiology. Renal physiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
5.2field-weighted citation impact, top 4% 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

48 citing papers in PubMed, 81 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Rare Variants in Genes Encoding Subunits of the Epithelial NaHypertension (Dallas, Tex. : 1979) · 2022
    Article
  11. Article
  12. Bile acids and salt-sensitive hypertension: a role of the gut-liver axis.American journal of physiology. Heart and circulatory physiology · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. 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 2 institutions in 1 country.

Tengis S PavlovDivision of Hypertension and Vascular Research, Henry Ford Hospital, Detroit, Michigan; and tpavlov1@hfhs.org.ORCID http://orcid.org/0000-0002-6481-0390
Alexander StaruschenkoDepartment of Physiology, Medical College of Wisconsin, Milwaukee, Wisconsin.ORCID http://orcid.org/0000-0002-5190-8356
Henry Ford Hospital · USMedical College of Wisconsin · US

Funding

Mechanisms and relevance of ENaC regulation by EGF and Rac1R01HL108880 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI STARUSCHENKO, ALEXANDER · 2012 to 2016
$1.9M
Role of NOX4 In Kidney Function In Salt-Sensitive HypertensionR01HL122662 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI COWLEY, ALLEN W, STARUSCHENKO, ALEXANDER · 2015 to 2018
$1.5M
Regulation of ENaC in salt-sensitive hypertension via inflammation-induced ROS productionR00HL116603 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI PAVLOV, TENGIS S · 2015 to 2017
$716k
Regulation of ENaC in salt-sensitive hypertension via inflammation-induced ROS prK99HL116603 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI PAVLOV, TENGIS S · 2013 to 2014
$180k
NHLBI NIH HHS K99 HL116603NHLBI NIH HHS R00 HL116603NHLBI NIH HHS R01 HL108880NHLBI NIH HHS R01 HL122662
6 · The paper itself

Abstract

Salt-sensitive hypertension is associated with renal and vascular dysfunctions, which lead to impaired fluid excretion, increased cardiac output, and total peripheral resistance. It is commonly accepted that increased renal sodium handling and plasma volume expansion are necessary factors for the development of salt-induced hypertension. The epithelial sodium channel (ENaC) is a trimeric ion channel expressed in the distal nephron that plays a critical role in the regulation of sodium reabsorption in both normal and pathological conditions. In this mini-review, we summarize recent studies investigating the role of ENaC in the development of salt-sensitive hypertension. On the basis of experimental data obtained from the Dahl salt-sensitive rats, we and others have demonstrated that abnormal ENaC activation in response to a dietary NaCl load contributes to the development of high blood pressure in this model. The role of different humoral factors, such as the components of the renin-angiotensin-aldosterone system, members of the epidermal growth factors family, arginine vasopressin, and oxidative stress mediating the effects of dietary salt on ENaC are discussed in this review to highlight future research directions and to determine potential molecular targets for drug development.

Indexed as

Blood PressureAnimalsArginine VasopressinDisease Models, AnimalEGF Family of ProteinsEpithelial CellsEpithelial Sodium ChannelsHumansHypertensionHypoglycemic AgentsMolecular Targeted TherapyNephronsOxidative StressRats, Inbred DahlRenal ReabsorptionRenin-Angiotensin SystemArginine VasopressinEGF Family of ProteinsEpithelial Sodium ChannelsHypoglycemic AgentsSodium Chloride, Dietary

Identifiers

PMID28003189
PMCPMC5582899
OpenAlexW2566597707

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.