Evidence map›Paper›PMID 19286591›Full record

ArticleStroke2009

Flow-induced dilation is mediated by Akt-dependent activation of endothelial nitric oxide synthase-derived hydrogen peroxide in mouse cerebral arteries.

Annick Drouin, Eric Thorin

Open access · bronzeAbstract read
In one paragraph

Article in Stroke, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.7field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 57 citations in OpenAlex.

  1. Hesperetin-7-Nutrients · 2023
    Trial
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Sex, Endothelial Cell Functions, and Peripheral Artery Disease.International journal of molecular sciences · 2023
    Review
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Microvascular NADPH oxidase in health and disease.Free radical biology & medicine · 2017
    Review
  15. Pulse pressure-dependent cerebrovascular eNOS regulation in mice.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2017
    Article
  16. Article
  17. Review
  18. Article
  19. Genetically engineered pig models for human diseases.Annual review of animal biosciences · 2013
    Review
  20. 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

2 authors at 1 institution in 1 country.

Annick DrouinInstitut de Cardiologie de Montréal, Centre de Recherche, Montréal, Québec, Canada.
Eric Thorin
Montreal Heart Institute · CA

Funding

CIHR 87388-1CIHR 89733-1
6 · The paper itself

Abstract

background and purposeEndothelial nitric oxide synthase produces superoxide under physiological conditions leading to hydrogen peroxide (H(2)O(2)) -dependent dilations to acetylcholine in isolated mouse cerebral arteries. The purpose of this study was to investigate whether H(2)O(2) was involved in flow-mediated dilation (FMD).

methodsCerebral arteries were isolated from 12+/-2-week-old C57Bl/6 male mice. FMD (0 to 10 microL/min, 2-microL step increase at constant internal pressure) was induced in vessels preconstricted with phenylephrine (30 micromol/L). Simultaneously to diameter acquisition, H(2)O(2) or nitric oxide production was detected by the fluorescent dyes CMH(2)CFDA or 4,5-diaminofluorescein diacetate, respectively. Results are expressed as mean+/-SEM of 6 to 8 mice.

resultsFMD (at 10 microL/min, 25+/-3% of maximal diameter) was prevented (P<0.05) by endothelium removal (6+/-1%) or endothelial nitric oxide synthase inhibition with N-nitro-L-arginine (11+/-1%) but not by the specific nitric oxide scavenger 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl3-oxide (24+/-3%). Addition of PEG-catalase and silver diethyl dithio-carbamate (superoxide dismutase inhibitor) reduced (P<0.05) FMD to 10+/-2% and 15+/-1%, respectively. Simultaneously to FMD, H(2)O(2)-associated rise in fluorescence (+133+/-19 a.u.) was prevented by N-nitro-L-arginine, PEG-catalase, and silver diethyl dithio-carbamate (+55+/-10, +64+/-4, and +50+/-10 a.u., respectively; P<0.05). Inhibition of FMD by PEG-catalase was fully restored by the addition of tetrahydrobiopterin, a cofactor of endothelial nitric oxide synthase (23+/-3%); this functional reversal in dilation was associated with the simultaneous increase in nitric oxide-associated fluorescence (+418+/-58 a.u., P<0.05), which was prevented by 2-phenyl-4,4,5,5-tetramethyl-imidazoline-1-oxyl3-oxide (+93+/-26 a.u.). Akt inhibition with triciribine prevented FMD and H(2)O(2)-associated rise in fluorescence (3+/-1% and +23+/-4% a.u., respectively; P<0.05), but not acetylcholine-induced dilation.

conclusionsIn healthy C57Bl/6 mouse cerebral arteries, Akt-dependent activation of endothelial nitric oxide synthase-derived H(2)O(2) mediates flow-dependent dilation.

Indexed as

AcetylcholineAnimalsBiopterinsCatalaseCerebral ArteriesCerebrovascular CirculationEnzyme ActivationEnzyme InhibitorsFluorescent DyesHydrogen PeroxideMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularNitric OxideNitric Oxide Synthase Type IIIAcetylcholineBiopterinsCatalaseEnzyme InhibitorsFluorescent DyesHydrogen PeroxideNitric OxideNitric Oxide Synthase Type IIIOncogene Protein v-aktsapropterinSuperoxide Dismutase

Identifiers

PMID19286591
PMCPMC3692461
OpenAlexW1969886567

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.