Evidence map›Paper›PMID 20018820›Full record

ArticleAmerican journal of physiology. Regulatory, integrative and comparative physiology2010

Asymmetric dimethylarginine in angiotensin II-induced hypertension.

Jennifer M Sasser, Natasha C Moningka, Mark W Cunningham, Byron Croker, Chris Baylis

Abstract read
In one paragraph

Article in American journal of physiology. Regulatory, integrative and comparative physiology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
4.2field-weighted citation impact, top 6% 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

34 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
  2. Article
  3. Oxidative Stress in Kidney Injury and Hypertension.Antioxidants (Basel, Switzerland) · 2024
    Review
  4. Article
  5. Blood pressure and albuminuria in a female mouse model of systemic lupus erythematosus: impact of long-term high salt consumption.American journal of physiology. Regulatory, integrative and comparative physiology · 2020
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Renal redox response to normal pregnancy in the rat.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  18. Article
  19. Renal microvascular dysfunction, hypertension and CKD progression.Current opinion in nephrology and hypertension · 2013
    Review
  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

5 authors at 3 institutions in 2 countries.

Jennifer M SasserDept. of Physiology and Functional Genomics, University of Florida, Gainesville, FL 32610, USA. jmsasser@ufl.edu
Natasha C Moningka
Mark W Cunningham
Byron Croker
Chris Baylis
Genomics (United Kingdom) · GBMalcom Randall VA Medical Center · USUniversity of Florida · US

Funding

Nitrix Oxide in Chronic Renal DiseaseR01DK056843 · NIDDK · WEST VIRGINIA UNIVERSITY · PI BAYLIS, CHRISTINE · 2001 to 2015
$3.4M
Multidisciplinary Training Program in HypertensionT32HL083810 · NHLBI · UNIVERSITY OF FLORIDA · PI WOOD, CHARLES E · 2007 to 2017
$2.5M
NHLBI NIH HHS T32 HL-083810NIDDK NIH HHS R01 DK-56843
6 · The paper itself

Abstract

Recent studies have shown that asymmetric dimethylarginine (ADMA), a nitric oxide synthase inhibitor, is increased in hypertension and chronic kidney disease. However, little is known about the effects of hypertension per se on ADMA metabolism. The purpose of this study was to test the hypothesis that ANG II-induced hypertension, in the absence of renal injury, is associated with increased oxidative stress and plasma and renal cortex ADMA levels in rats. Male Sprague-Dawley rats were treated with ANG II at 200 ng.kg(-1).min(-1) sc (by minipump) for 1 or 3 wk or at 400 ng.kg(-1).min(-1) for 6 wk. Mean arterial pressure was increased after 3 and 6 wk of ANG II; however, renal injury (proteinuria, glomerular sclerosis, and interstitial fibrosis) was only evident after 6 wk of treatment. Plasma thiobarbituric acid reactive substances concentration and renal cortex p22(phox) protein abundance were increased early (1 and 3 wk), but urinary excretion of isoprostane and H(2)O(2) was only increased after 6 wk of ANG II. An increased in plasma ADMA after 6 wk of ANG II was associated with increased lung protein arginine methyltransferase-1 abundance and decreased renal cortex dimethylarginine dimethylaminohydrolase activity. No changes in renal cortex ADMA were observed. ANG II hypertension in the absence of renal injury is not associated with increased ADMA; however, when the severity and duration of the treatment were increased, plasma ADMA increased. These data suggest that elevated blood pressure alone, for up to 3 wk, in the absence of renal injury does not play an important role in the regulation of ADMA. However, the presence of renal injury and sustained hypertension for 6 wk increases ADMA levels and contributes to nitric oxide deficiency and cardiovascular disease.

Indexed as

AmidohydrolasesAngiotensin IIAnimalsArginineBlood PressureFibrosisHypertension, RenalKidney CortexMaleNADPH OxidasesNitratesNitritesOxidative StressProtein-Arginine N-MethyltransferasesRatsRats, Sprague-DawleyAmidohydrolasesAngiotensin IIArginineCyba protein, ratdimethylargininaseNADPH OxidasesNitratesNitritesN,N-dimethylargininePRMT1 protein, ratProtein-Arginine N-MethyltransferasesThiobarbituric Acid Reactive SubstancesVasoconstrictor Agents

Identifiers

PMID20018820
PMCPMC2838660
OpenAlexW2159347027

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.