Evidence map›Paper›PMID 25298524›Full record

ArticleAmerican journal of physiology. Renal physiology2014

Serelaxin reduces oxidative stress and asymmetric dimethylarginine in angiotensin II-induced hypertension.

Jennifer M Sasser, Mark W Cunningham, Chris Baylis

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.4field-weighted citation impact, top 3% 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

23 citing papers in PubMed, 51 citations in OpenAlex.

  1. Review
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  11. Relaxin-mediated renal vasodilation in the rat is associated with falls in glomerular blood pressure.American journal of physiology. Regulatory, integrative and comparative physiology · 2018
    Article
  12. Article
  13. Review
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  15. The Role of Genetics in Peripartum Cardiomyopathy.Journal of cardiovascular translational research · 2017
    Review
  16. Article
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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.

Jennifer M SasserDepartment of Pharmacology and Toxicology, University of Mississippi Medical Center, Jackson, Mississippi; Department of Physiology and Functional Genomics, University of Florida, Gainesville, Florida; and jsasser@umc.edu.
Mark W CunninghamDepartment of Physiology and Functional Genomics, University of Florida, Gainesville, Florida; and.
Chris BaylisDepartment of Physiology and Functional Genomics, University of Florida, Gainesville, Florida; and Department of Medicine, University of Florida, Gainesville, Florida.
University of Florida · USUniversity of Mississippi Medical Center · US

Funding

Hypertension and Cardiorenal Research Training ProgramT32HL105324 · NHLBI · UNIVERSITY OF MISSISSIPPI MED CTR · PI Joey P. Granger · 2010 to 2026
$7.8M
Nitrix Oxide in Chronic Renal DiseaseR01DK056843 · NIDDK · WEST VIRGINIA UNIVERSITY · PI BAYLIS, CHRISTINE · 2001 to 2015
$3.4M
Mechanisms of Renoprotection by Relaxin in HypertensionK01DK095018 · NIDDK · UNIVERSITY OF MISSISSIPPI MED CTR · PI SASSER, JENNIFER M · 2012 to 2016
$634k
NHLBI NIH HHS T32 HL105324NIDDK NIH HHS K01 DK095018NIDDK NIH HHS R01 DK056843NIDDK NIH HHS R01 DK56843
6 · The paper itself

Abstract

Recent findings suggest the therapeutic action of relaxin during hypertension is dependent on nitric oxide synthase (NOS) activation; however, the mechanisms underlying the beneficial effects of relaxin on the NOS system have not been fully elucidated. We hypothesized that the protective effects of relaxin include reducing both oxidative stress and the endogenous NOS inhibitor asymmetric dimethylarginine (ADMA). We examined the effect of Serelaxin [human recombinant relaxin-2 (RLX)] in male Sprague-Dawley rats given high-dose angiotensin (ANG) II (400 ng·kg(-1)·min(-1) sc) for 6 wk or shams. RLX was administered (4 μg/h sc) to half of the rats in each group after 2 wk of ANG II for the remaining 4 wk. ANG II induced hypertension and proteinuria, reduced NO oxidation products (NOx), and increased oxidative stress (NADPH oxidase activity, thiobarbituric acid-reactive substances, and 8-isoprostane excretion) and plasma ADMA. While RLX had no effect on sham rats, RLX attenuated the ANG II-dependent hypertension (165 ± 5 vs. 135 ± 13 mmHg, P < 0.05) and proteinuria at 6 wk (62 ± 6 vs. 41 ± 4 mg·day(-1)·100 g(-1), P < 0.05) and normalized oxidative stress and circulating ADMA, in association with restored NOx excretion and kidney cortex NOx. We found that RLX had no impact on the ADMA-regulatory enzymes protein arginine methyltransferase and dimethylarginine-dimethylaminohydrolase (DDAH). Furthermore, RLX treatment did not increase DDAH activity in kidney cortex or liver. These data suggest that benefits of RLX treatment include reduced ADMA levels and increased NO bioavailability, possibly due to its antioxidant effects.

Indexed as

Angiotensin IIAnimalsAntihypertensive AgentsAntioxidantsArginineArterial PressureDinoprostDisease Models, AnimalDown-RegulationHumansHypertensionInjections, SubcutaneousKidneyLiverMaleNADPH Oxidases8-epi-prostaglandin F2alphaAngiotensin IIAntihypertensive AgentsAntioxidantsArginineDinoprostNADPH OxidasesNitric OxideN,N-dimethylarginineRecombinant ProteinsRelaxinserelaxin protein, humanThiobarbituric Acid Reactive Substancesdimethylarginine dimethylaminohydrolaseNADPH oxidasenitric oxideprotein arginine methyltransferase-1

Identifiers

PMID25298524
PMCPMC4269693
OpenAlexW2327992730

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.