Evidence map›Paper›PMID 19592567›Full record

ArticleCardiovascular research2009

Ascorbic acid and tetrahydrobiopterin potentiate the EDHF phenomenon by generating hydrogen peroxide.

Ambroise Garry, David H Edwards, Ian F Fallis, Robert L Jenkins, Tudor M Griffith

Open access · greenAbstract read
In one paragraph

Article in Cardiovascular research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
6.0field-weighted citation impact, top 4% 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

20 citing papers in PubMed, 45 citations in OpenAlex.

  1. BH4 Oxidation-Derived HJournal of neurochemistry · 2025
    Article
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  4. Update on the role of endothelial cells in trauma.European journal of trauma and emergency surgery : official publication of the European Trauma Society · 2018
    Review
  5. Article
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  7. Article
  8. Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Tetrahydrobiopterin increases NO-dependent vasodilation in hypercholesterolemic human skin through eNOS-coupling mechanisms.American journal of physiology. Regulatory, integrative and comparative physiology · 2013
    Article
  14. Article
  15. Review
  16. Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

5 authors at 1 institution in 1 country.

Ambroise GarryDepartment of Diagnostic Radiology, Wales Heart Research Institute, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
David H Edwards
Ian F Fallis
Robert L Jenkins
Tudor M Griffith
Cardiff University · GB

Funding

British Heart Foundation PG/05/133/19892
6 · The paper itself

Abstract

aimsOur objective was to investigate whether pro-oxidant properties of ascorbic acid (AA) and tetrahydrobiopterin (BH(4)) modulate endothelium-dependent, electrotonically mediated arterial relaxation. METHODS AND

resultsIn studies with rabbit iliac artery (RIA) rings, NO-independent, endothelium-derived hyperpolarizing factor (EDHF)-type relaxations evoked by the sarcoplasmic endoplasmic reticulum Ca(2+)-ATPase inhibitor cyclopiazonic acid and the G protein-coupled agonist acetylcholine (ACh) were enhanced by AA (1 mM) and BH(4) (200 microM), which generated buffer concentrations of H(2)O(2) in the range of 40-80 microM. Exogenous H(2)O(2) potentiated cyclopiazonic acid (CPA)- and ACh-evoked relaxations with a threshold of 10-30 microM, and potentiation by AA and BH(4) was abolished by catalase, which destroyed H(2)O(2) generated by oxidation of these agents in the organ chamber. Adventitial application of H(2)O(2) also enhanced EDHF-type dilator responses evoked by CPA and ACh in RIA segments perfused intraluminally with H(2)O(2)-free buffer, albeit with reduced efficacy. In RIA rings, both control relaxations and their potentiation by H(2)O(2) were overcome by blockade of gap junctions by connexin-mimetic peptides (YDKSFPISHVR and SRPTEK) targeted to the first and second extracellular loops of the dominant vascular connexins expressed in the RIA. Superoxide dismutase attenuated the potentiation of EDHF-type relaxations by BH(4), but not AA, consistent with findings demonstrating a differential role for superoxide anions in the generation of H(2)O(2) by the two agents.

conclusionPro-oxidant effects of AA and BH(4) can enhance the EDHF phenomenon by generating H(2)O(2), which has previously been shown to amplify electrotonic hyperpolarization-mediated relaxation by facilitating Ca(2+) release from endothelial stores.

Indexed as

AcetylcholineAnimalsAscorbic AcidBiological FactorsBiopterinsCalciumCatalaseConnexinsDose-Response Relationship, DrugGap JunctionsHydrogen PeroxideIliac ArteryIndolesIn Vitro TechniquesMaleOxidantsAcetylcholineAscorbic AcidBiological FactorsBiopterinsCalciumCatalaseConnexinscyclopiazonic acidendothelium-dependent hyperpolarization factorHydrogen PeroxideIndolesOxidantsPeptidessapropterinSarcoplasmic Reticulum Calcium-Transporting ATPasesSuperoxide DismutaseSuperoxidesVasodilator Agents

Identifiers

PMID19592567
PMCPMC2761203
OpenAlexW2111068518

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.