Evidence map›Paper›PMID 20424940›Full record

ReviewCurrent hypertension reports2010

Modulation of pressure-natriuresis by renal medullary reactive oxygen species and nitric oxide.

Paul M O'Connor, Allen W Cowley

Abstract readReview
In one paragraph

Review in Current hypertension reports, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.6field-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

33 citing papers in PubMed, 63 citations in OpenAlex.

  1. Review
  2. Article
  3. Renal Medulla in Hypertension.Hypertension (Dallas, Tex. : 1979) · 2024
    Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. NOX4-dependent regulation of ENaC in hypertension and diabetic kidney disease.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  9. Review
  10. Article
  11. Article
  12. Involvement of ENaC in the development of salt-sensitive hypertension.American journal of physiology. Renal physiology · 2017
    Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. High salt induces autocrine actions of ET-1 on inner medullary collecting duct NO production via upregulated ETB receptor expression.American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Article
  18. Proton channels and renal hypertensive injury: a key piece of the Dahl salt-sensitive rat puzzle?American journal of physiology. Regulatory, integrative and comparative physiology · 2016
    Review
  19. Article
  20. Activators of G protein signaling in the kidney.The Journal of pharmacology and experimental therapeutics · 2015
    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.

Paul M O'ConnorDepartment of Physiology, Medical College of Wisconsin, Milwaukee, WI 53202, USA. poconnor@mcw.edu
Allen W Cowley
Medical College of Wisconsin · US

Funding

VASOPRESSIN SECRETION AND CARDIOVASCULAR FUNCTIONP01HL029587 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI COWLEY, ALLEN W · 1985 to 2012
$24.1M
Research ServicesP01HL082798 · NHLBI · MEDICAL COLLEGE OF WISCONSIN · PI GREENE, ANDREW S. · 2006 to 2015
$22.0M
NHLBI NIH HHS P01 HL029587NHLBI NIH HHS P01 HL082798
6 · The paper itself

Abstract

The renal pressure-natriuresis mechanism is the dominant controller of body fluid balance and long-term arterial pressure. In recent years, it has become clear that the balance of reactive oxygen and nitrogen species within the renal medullary region is a key determinant of the set point of the renal pressure-natriuresis curve. The development of renal medullary oxidative stress causes dysfunction of the pressure-natriuresis mechanism and contributes to the development of hypertension in numerous disease models. The purpose of this review is to point out the known mechanisms within the renal medulla through which reactive oxygen and nitrogen species modulate the pressure-natriuresis response and to update the reader on recent advances in this field.

Indexed as

NatriuresisReactive Oxygen SpeciesBlood PressureDiuresisEndothelinsEndothelium-Dependent Relaxing FactorsEndothelium, VascularHumansHydrogen PeroxideKidney MedullaNitric OxideNitric Oxide SynthaseOxidative StressSignal TransductionSodium, DietarySuperoxidesEndothelinsEndothelium-Dependent Relaxing FactorsHydrogen PeroxideNitric OxideNitric Oxide SynthaseReactive Oxygen SpeciesSodium, DietarySuperoxides

Identifiers

PMID20424940
PMCPMC3722865
OpenAlexW1965843452

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.