Evidence map›Paper›PMID 20558825›Full record

ArticleCirculation research2010

Nitro-oleic acid inhibits angiotensin II-induced hypertension.

Jifeng Zhang, Luis Villacorta, Lin Chang, Zhenzhen Fan, Milton Hamblin, Tianqing Zhu, Chen S Chen, Marsha P Cole, Francisco J Schopfer, Cheri X Deng and 4 more

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Circulation research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 75 papers.

0numbers the graph read from it
0cells of the map it votes in
75citing papers in PubMed
7.7field-weighted citation impact, top 2% 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

75 citing papers in PubMed, 121 citations in OpenAlex.

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  11. Bioactive lipids in hypertension.Advances in pharmacology (San Diego, Calif.) · 2023
    Article
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  15. Antihypertensive potential ofFrontiers in pharmacology · 2022
    Article
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  20. Review

15 more citing papers are in PubMed but not listed here.

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

14 authors at 4 institutions in 3 countries.

Jifeng ZhangCardiovascular Center, College of Engineering, University of Michigan, USA.
Luis Villacorta
Lin Chang
Zhenzhen Fan
Milton Hamblin
Tianqing Zhu
Chen S Chen
Marsha P Cole
Francisco J Schopfer
Cheri X Deng
Minerva T Garcia-Barrio
Ying-Hong Feng
Bruce A Freeman
Y Eugene Chen
Cardiovascular Institute Hospital · JPMorehouse School of Medicine · USCardiovascular Research Center · BRUniversity of Michigan–Ann Arbor · US

Funding

The Role of PPAR-gamma in Vascular Lesion FormationR01HL068878 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2002 to 2019
$7.6M
Redox-Derived Pulmonary Anti-Inflammatory MediatorsR01HL064937 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2000 to 2015
$5.6M
Redox Transduction of Nitric Oxide SignalingR37HL058115 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 2008 to 2017
$5.2M
NITRIC OXIDE REGULATION OF VASCULAR OXIDANT INJURYR01HL058115 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI FREEMAN, BRUCE ALAN · 1998 to 2007
$3.3M
Advanced Ultrasound Ablation Therapy for Atrial FibrillationR01EB008999 · NIBIB · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DENG, CHERI X · 2008 to 2012
$2.8M
Nitro-Fatty Acids and Nrf2 in Vascular RemodelingR01HL105114 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2010 to 2014
$2.6M
Nitroalkenes and Blood Pressure RegulationR01HL089544 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2008 to 2012
$2.0M
CRP Biology and Vascular DiseaseR01HL088391 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING EUGENE · 2009 to 2013
$1.8M
PPAR-delta in obesity-related vascular remodelingR01HL075397 · NHLBI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI CHEN, YUQING E · 2004 to 2007
$1.7M
Mechanisms of ultrasound mediated intracellular drug and gene deliveryR01CA116592 · NCI · UNIVERSITY OF MICHIGAN AT ANN ARBOR · PI DENG, CHERI X · 2005 to 2009
$1.4M
Metabolic Stress-Induced Fatty Acid Nitration and Cardiovascular FunctionK99HL095769 · NHLBI · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI COLE, MARSHA P · 2010 to 2011
$145k
NCI NIH HHS CA116592NCI NIH HHS R01 CA116592NHLBI NIH HHS HL089544NHLBI NIH HHS HL58115NHLBI NIH HHS HL64937NHLBI NIH HHS HL68878NHLBI NIH HHS K99 HL095769NHLBI NIH HHS R01 HL058115NHLBI NIH HHS R01 HL064937NHLBI NIH HHS R01 HL068878NHLBI NIH HHS R01 HL075397NHLBI NIH HHS R01 HL088391NHLBI NIH HHS R01 HL089544NHLBI NIH HHS R01 HL105114NHLBI NIH HHS R37 HL058115NIBIB NIH HHS R01 EB008999
6 · The paper itself

Abstract

rationaleNitro-oleic acid (OA-NO(2)) is a bioactive, nitric-oxide derived fatty acid with physiologically relevant vasculoprotective properties in vivo. OA-NO(2) exerts cell signaling actions as a result of its strong electrophilic nature and mediates pleiotropic cell responses in the vasculature.

objectiveThe present study sought to investigate the protective role of OA-NO(2) in angiotensin (Ang) II-induced hypertension. METHODS AND

resultsWe show that systemic administration of OA-NO(2) results in a sustained reduction of Ang II-induced hypertension in mice and exerts a significant blood pressure lowering effect on preexisting hypertension established by Ang II infusion. OA-NO(2) significantly inhibits Ang II contractile response as compared to oleic acid (OA) in mesenteric vessels. The improved vasoconstriction is specific for the Ang II type 1 receptor (AT(1)R)-mediated signaling because vascular contraction by other G-protein-coupled receptors is not altered in response to OA-NO(2) treatment. From the mechanistic viewpoint, OA-NO(2) lowers Ang II-induced hypertension independently of peroxisome proliferation-activated receptor (PPAR)gamma activation. Rather, OA-NO(2), but not OA, specifically binds to the AT(1)R, reduces heterotrimeric G-protein coupling, and inhibits IP(3) (inositol-1,4,5-trisphosphate) and calcium mobilization, without inhibiting Ang II binding to the receptor.

conclusionsThese results demonstrate that OA-NO(2) diminishes the pressor response to Ang II and inhibits AT(1)R-dependent vasoconstriction, revealing OA-NO(2) as a novel antagonist of Ang II-induced hypertension.

Indexed as

Angiotensin IIAnimalsBlood PressureHypertensionLinoleic AcidsMiceMice, Inbred C57BLNitro CompoundsOleic AcidOleic AcidsRatsRats, Sprague-Dawley10-nitro-9,12-octadecadienoic acid10-nitro-oleic acidAngiotensin IILinoleic AcidsNitro CompoundsOleic AcidOleic Acids

Identifiers

PMID20558825
PMCPMC2937264
OpenAlexW2097005377

What OpenQuestion holds

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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.