Evidence map›Paper›PMID 18487445›Full record

ArticleAmerican journal of physiology. Heart and circulatory physiology2008

Xanthine oxidase and mitochondria contribute to vascular superoxide anion generation in DOCA-salt hypertensive rats.

Emilie C Viel, Karim Benkirane, Danesh Javeshghani, Rhian M Touyz, Ernesto L Schiffrin

Abstract read
In one paragraph

Article in American journal of physiology. Heart and circulatory physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
4.3field-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

41 citing papers in PubMed, 114 citations in OpenAlex.

  1. Trial
  2. Reactive oxygen species in hypertension.Nature reviews. Cardiology · 2025
    Review
  3. Review
  4. Oxidative Stress, Antioxidants and Hypertension.Antioxidants (Basel, Switzerland) · 2023
    Review
  5. Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022
    Review
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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

5 authors at 1 institution in 1 country.

Emilie C VielLady Davis Institute for Medical Research, Montreal, QC, Canada H3T 1E2.
Karim Benkirane
Danesh Javeshghani
Rhian M Touyz
Ernesto L Schiffrin
Jewish General Hospital · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Vascular superoxide anion (O(2)(*-)) levels are increased in DOCA-salt hypertensive rats. We hypothesized that the endothelin (ET)-1-induced generation of ROS in the aorta and resistance arteries of DOCA-salt rats originates partly from xanthine oxidase (XO) and mitochondria. Accordingly, we blocked XO and the mitochondrial oxidative phosphorylation chain to investigate their contribution to ROS production in mesenteric resistance arteries and the aorta from DOCA-salt rats. Systolic blood pressure rose in DOCA-salt rats and was reduced after 3 wk by apocynin [NAD(P)H oxidase inhibitor and/or radical scavenger], allopurinol (XO inhibitor), bosentan (ET(A/B) receptor antagonist), BMS-182874 (BMS; ET(A) receptor antagonist), and hydralazine. Plasma uric acid levels in DOCA-salt rats were similar to control unilaterally nephrectomized (UniNx) rats, reduced with allopurinol and bosentan, and increased with BMS. Levels of thiobarbituric acid-reacting substances were increased in DOCA-salt rats versus UniNx rats, and BMS, bosentan, and hydralazine prevented their increase. Dihydroethidium staining showed reduced O(2)(*-) production in mesenteric arteries and the aorta from BMS- and bosentan-treated DOCA-salt rats compared with untreated DOCA-salt rats. Increased O(2)(*-) derived from XO was reduced or prevented by all treatments in mesenteric arteries, whereas bosentan and BMS had no effect on aortas from DOCA-salt rats. O(2)(*-) generation decreased with in situ treatment by tenoyltrifluoroacetone and CCCP, inhibitors of mitochondrial electron transport complexes II and IV, respectively, whereas rotenone (mitochondrial complex I inhibitor) had no effect. Our findings demonstrate the involvement of ET(A) receptor-modulated O(2)(*-) derived from XO and from mitochondrial oxidative enzymes in arteries from DOCA-salt rats.

Indexed as

AnimalsAntihypertensive AgentsAortaBlood PressureCreatinineDesoxycorticosteroneDisease Models, AnimalEndothelin-1Endothelin Receptor AntagonistsEnzyme InhibitorsFree Radical ScavengersHypertensionLipid PeroxidationMaleMesenteric ArteriesMitochondriaAntihypertensive AgentsCreatinineDesoxycorticosteroneEndothelin-1Endothelin Receptor AntagonistsEnzyme InhibitorsFree Radical ScavengersNADPH OxidasesReceptors, EndothelinSuperoxidesThiobarbituric Acid Reactive SubstancesUncoupling AgentsUric AcidXanthine Oxidase

Identifiers

PMID18487445
PMCPMC2494748
OpenAlexW2156106643

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.