Evidence map›Paper›PMID 26028244›Full record

ReviewCurrent hypertension reviews2015

Salt-Sensitive Hypertension: Perspectives on Intrarenal Mechanisms.

Dewan S A Majid, Minolfa C Prieto, Luis Gabriel Navar

Open access · greenAbstract readReview
In one paragraph

Review in Current hypertension reviews, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
5.4field-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

50 citing papers in PubMed, 74 citations in OpenAlex.

  1. Trial
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  4. Sex differences in the progression of salt-sensitive hypertension in aged Dahl salt-sensitive rats.American journal of physiology. Regulatory, integrative and comparative physiology · 2026
    Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Early-life sodium restriction programs autonomic dysfunction and salt sensitivity in male C57BL/6J mice.American journal of physiology. Regulatory, integrative and comparative physiology · 2025
    Article
  13. Review
  14. Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024
    Review
  15. Article
  16. Article
  17. The role of NaPflugers Archiv : European journal of physiology · 2024
    Review
  18. Article
  19. T helper cell polarity determines salt sensitivity and hypertension development.Hypertension research : official journal of the Japanese Society of Hypertension · 2023
    Article
  20. Oxidative medicine and cellular longevity · 2023
    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

3 authors at 1 institution in 1 country.

Dewan S A MajidDepartment of Physiology, SL39, Tulane University School of Medicine, 1430 Tulane Avenue, New Orleans, LA 70112, USA. majid@tulane.edu.
Minolfa C Prieto
Luis Gabriel Navar
Tulane University · US

Funding

Translational Research in Hypertension and Renal BiologyP30GM103337 · NIGMS · TULANE UNIVERSITY OF LOUISIANA · PI NAVAR, LUIS GABRIEL · 2012 to 2016
$5.8M
Superoxide and nitric Oxide Interactions in the KidneyR01HL066432 · NHLBI · TULANE UNIVERSITY OF LOUISIANA · PI MAJID, DEWAN SYED ABDUL · 2001 to 2012
$3.0M
PLEIOTROPIC EFFECTS OF PRORENIN RECEPOR IN COLLECTING DUCT AND INTRARENAL RAS ACTIVATIONR01DK104375 · NIDDK · TULANE UNIVERSITY OF LOUISIANA · PI PRIETO, MINOLFA C · 2014 to 2018
$1.7M
NHLBI NIH HHS HL-66432NHLBI NIH HHS R01 HL066432NIDDK NIH HHS R01 DK104375NIGMS NIH HHS P30 GM103337NIGMS NIH HHS P30GM103337
6 · The paper itself

Abstract

Salt sensitive hypertension is characterized by increases in blood pressure in response to increases in dietary salt intake and is associated with an enhanced risk of cardiovascular and renal morbidity. Although researchers have sought for decades to understand how salt sensitivity develops in humans, the mechanisms responsible for the increases in blood pressure in response to high salt intake are complex and only partially understood. Until now, scientists have been unable to explain why some individuals are salt sensitive and others are salt resistant. Although a central role for the kidneys in the development of salt sensitivity and hypertension has been generally accepted, it is also recognized that hypertension is of multifactorial origin and a variety of factors can induce, or prevent, blood pressure responsiveness to the manipulation of salt intake. Excess salt intake in susceptible persons may also induce inappropriate central and sympathetic nervous system responses and increase the production of intrarenal angiotensin II, catecholamines and other factors such as oxidative stress and inflammatory cytokines. One key factor is the concomitant inappropriate or paradoxical activation of the intrarenal renin-angiotensin system, by high salt intake. This is reflected by the increases in urinary angiotensinogen during high salt intake in salt sensitive models. A complex interaction between neuroendocrine factors and the kidney may underlie the propensity for some individuals to retain salt and develop salt-dependent hypertension. In this review, we focus mainly on the renal contributions that provide the mechanistic links between chronic salt intake and the development of hypertension.

Indexed as

Angiotensin IIAngiotensinsAnimalsBlood PressureHumansHypertensionKidneyKidney Tubules, ProximalModels, BiologicalOxidative StressRenin-Angiotensin SystemSodium, DietaryAngiotensin IIAngiotensinsSodium, Dietary

Identifiers

PMID26028244
PMCPMC4626881
OpenAlexW2123532936

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.