Evidence map›Paper›PMID 21955547›Full record

ArticleBMC pharmacology2011

Protection of protease-activated receptor 2 mediated vasodilatation against angiotensin II-induced vascular dysfunction in mice.

Elizabeth Chia, Satomi Kagota, Enoka P Wijekoon, John J McGuire

Open access · hybridAbstract read
In one paragraph

Article in BMC pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 19% 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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 22 citations in OpenAlex.

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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

4 authors at 2 institutions in 2 countries.

Elizabeth ChiaMemorial University, St, John's, Newfoundland and Labrador, Canada.
Satomi Kagota
Enoka P Wijekoon
John J McGuire
Memorial University of Newfoundland · CAUniversity of Guelph · CA

Funding

Canadian Institutes of Health Research R0P-72465Canadian Institutes of Health Research R0P-88065Canadian Institutes of Health Research RSH-78370
6 · The paper itself

Abstract

backgroundUnder conditions of cardiovascular dysfunction, protease-activated receptor 2 (PAR2) agonists maintain vasodilatation activity, which has been attributed to increased cyclooxygenase-2, nitric oxide synthase and calcium-activated potassium channel (SK3.1) activities. Protease-activated receptor 2 agonist mediated vasodilatation is unknown under conditions of dysfunction caused by angiotensin II. The main purpose of our study was to determine whether PAR2-induced vasodilatation of resistance arteries was attenuated by prolonged angiotensin II treatment in mice. We compared the vasodilatation of resistance-type arteries (mesenteric) from angiotensin II-treated PAR2 wild-type mice (WT) induced by PAR2 agonist 2-furoyl-LIGRLO-amide (2fly) to the responses obtained in controls (saline treatment). We also investigated arterial vasodilatation in angiotensin II-treated PAR2 deficient (PAR2-/-) mice.

results2fly-induced relaxations of untreated arteries from angiotensin II-treated WT were not different than saline-treated WT. Treatment of arteries with nitric oxide synthase inhibitor and SK3.1 inhibitor (L-NAME + TRAM-34) blocked 2fly in angiotensin II-treated WT. Protein and mRNA expression of cyclooxygenase-1 and -2 were increased, and cyclooxygenase activity increased the sensitivity of arteries to 2fly in only angiotensin II-treated WT. These protective vasodilatation mechanisms were selective for 2fly compared with acetylcholine- and nitroprusside-induced relaxations which were attenuated by angiotensin II; PAR2-/- were protected against this attenuation of nitroprusside.

conclusionsPAR2-mediated vasodilatation of resistance type arteries is protected against the negative effects of angiotensin II-induced vascular dysfunction in mice. In conditions of endothelial dysfunction, angiotensin II induction of cyclooxygenases increases sensitivity to PAR2 agonist and the preserved vasodilatation mechanism involves activation of SK3.1.

Indexed as

AcetylcholineAngiotensin IIAnimalsBlotting, WesternCyclooxygenase 1Cyclooxygenase 2Dose-Response Relationship, DrugEndothelium, VascularGene ExpressionIn Vitro TechniquesMaleMesenteric ArteriesMiceMice, Inbred C57BLMice, KnockoutNG-Nitroarginine Methyl Ester2-furoyl-LIGRLO-amideAcetylcholineAngiotensin IICyclooxygenase 1Cyclooxygenase 2Kcnn3 protein, mouseNG-Nitroarginine Methyl EsterNitric Oxide SynthaseNitroprussideOligopeptidesPyrazolesReceptor, PAR-2Small-Conductance Calcium-Activated Potassium ChannelsTRAM 34Vasoconstrictor AgentsVasodilator Agents

Identifiers

PMID21955547
PMCPMC3192660
OpenAlexW2077188624

What OpenQuestion holds

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LicenceCC BY
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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.