Evidence map›Paper›PMID 25093847›Full record

ArticlePloS one2014

Hydrogen peroxide elicits constriction of skeletal muscle arterioles by activating the arachidonic acid pathway.

Viktória Csató, Attila Pető, Ákos Koller, István Édes, Attila Tóth, Zoltán Papp

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.3field-weighted citation impact, top 36% 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

4 citing papers in PubMed, 5 citations in OpenAlex.

  1. Article
  2. Oxidative Regulation of Vascular CaAntioxidants (Basel, Switzerland) · 2022
    Review
  3. Article
  4. 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

6 authors at 2 institutions in 2 countries.

Viktória CsatóDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary; Research Centre for Molecular Medicine, University of Debrecen, Debrecen, Hungary.
Attila PetőDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary; Research Centre for Molecular Medicine, University of Debrecen, Debrecen, Hungary.
Ákos KollerDepartment of Pathophysiology and Gerontology, University of Pécs, Pécs, Hungary; Department of Pathophysiology, Semmelweis University, Budapest, Hungary; Department of Physiology, New York Medical College, Valhalla, New York, United States of America.
István ÉdesDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary; Research Centre for Molecular Medicine, University of Debrecen, Debrecen, Hungary.
Attila TóthDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary; Research Centre for Molecular Medicine, University of Debrecen, Debrecen, Hungary.
Zoltán PappDivision of Clinical Physiology, Institute of Cardiology, University of Debrecen, Debrecen, Hungary; Research Centre for Molecular Medicine, University of Debrecen, Debrecen, Hungary.
University of Debrecen · HUNew York Medical College · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

aimsThe molecular mechanisms of the vasoconstrictor responses evoked by hydrogen peroxide (H2O2) have not been clearly elucidated in skeletal muscle arterioles. METHODS AND

resultsChanges in diameter of isolated, cannulated and pressurized gracilis muscle arterioles (GAs) of Wistar-Kyoto rats were determined under various test conditions. H2O2 (10-100 µM) evoked concentration-dependent constrictions in the GAs, which were inhibited by endothelium removal, or by antagonists of phospholipase A (PLA; 100 µM 7,7-dimethyl-(5Z,8Z)-eicosadienoic acid), protein kinase C (PKC; 10 µM chelerythrine), phospholipase C (PLC; 10 µM U-73122), or Src family tyrosine kinase (Src kinase; 1 µM Src Inhibitor-1). Antagonists of thromboxane A2 (TXA2; 1 µM SQ-29548) or the non-specific cyclooxygenase (COX) inhibitor indomethacin (10 µM) converted constrictions to dilations. The COX-1 inhibitor (SC-560, 1 µM) demonstrated a greater reduction in constriction and conversion to dilation than that of COX-2 (celecoxib, 3 µM). H2O2 did not elicit significant changes in arteriolar Ca(2+) levels measured with Fura-2.

conclusionsThese data suggest that H2O2 activates the endothelial Src kinase/PLC/PKC/PLA pathway, ultimately leading to the synthesis and release of TXA2 by COX-1, thereby increasing the Ca(2+) sensitivity of the vascular smooth muscle cells and eliciting constriction in rat skeletal muscle arterioles.

Indexed as

AnimalsArachidonic AcidArteriolesCoronary VesselsEndothelium, VascularHeartHydrogen PeroxideMaleMetabolic Networks and PathwaysMuscle, SkeletalRatsRats, WistarVasoconstrictionArachidonic AcidHydrogen Peroxide

Identifiers

PMID25093847
PMCPMC4122381
OpenAlexW2157526268

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.