Evidence map›Paper›PMID 23145049›Full record

ArticlePloS one2012

Low mercury concentration produces vasoconstriction, decreases nitric oxide bioavailability and increases oxidative stress in rat conductance artery.

Núbia Belem Lemos, Jhuli Keli Angeli, Thaís de Oliveira Faria, Eduardo Hertel Ribeiro, Dalton Valentim Vassallo, Alessandra Simão Padilha, Ivanita Stefanon

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 11% 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

15 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.

  1. Pooled it
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  14. Inhibition of As(III) and Hg(II) caused aortic hypercontraction by eugenol, linalool and carvone.Journal of smooth muscle research = Nihon Heikatsukin Gakkai kikanshi · 2014
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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

7 authors at 1 institution in 1 country.

Núbia Belem LemosDepartamento de Ciências Fisiológicas, Universidade Federal do Espírito Santo, Vitória, Espírito Santo, Brazil.
Jhuli Keli Angeli
Thaís de Oliveira Faria
Eduardo Hertel Ribeiro
Dalton Valentim Vassallo
Alessandra Simão Padilha
Ivanita Stefanon
Universidade Federal do Espírito Santo · BR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mercury is an environmental pollutant that reduces nitric oxide (NO) bioavailability and increases oxidative stress, having a close link with cardiovascular diseases, as carotid atherosclerosis, myocardial infarction, coronary heart disease and hypertension. One of the main sites affected by oxidative stress, which develops atherosclerosis, is the aorta. Under acute exposure to low mercury concentrations reactive oxygen species (ROS) production were only reported for resistance vessels but if low concentrations of mercury also affect conductance arteries it is still unclear. We investigated the acute effects of 6 nM HgCl(2) on endothelial function of aortic rings measuring the reactivity to phenylephrine in rings incubated, or not, with HgCl(2) for 45 min, the protein expression for cyclooxygenase 2 (COX-2) and the AT1 receptor. HgCl(2) increased Rmax and pD2 to phenylephrine without changing the vasorelaxation induced by acetylcholine and sodium nitroprusside. Endothelial damage abolished the increased reactivity to phenylephrine. The increase of Rmax and pD2 produced by L-NAME was smaller in the presence of HgCl(2). Enalapril, losartan, indomethacin, furegrelate, the selective COX-2 inhibitor NS 398, superoxide dismutase and the NADPH oxidase inhibitor apocynin reverted HgCl(2) effects on the reactivity to phenylephrine, COX-2 protein expression was increased, and AT1 expression reduced. At low concentration, below the reference values, HgCl(2) increased vasoconstrictor activity by reducing NO bioavailability due to increased ROS production by NADPH oxidase activity. Results suggest that this is due to local release of angiotensin II and prostanoid vasoconstrictors. Results also suggest that acute low concentration mercury exposure, occurring time to time could induce vascular injury due to endothelial oxidative stress and contributing to increase peripheral resistance, being a high risk factor for public health.

Indexed as

AcetylcholineAnimalsArteriesBiological AvailabilityCyclooxygenase 2Cyclooxygenase 2 InhibitorsEndothelium, VascularFree RadicalsMaleMercuryNADPH OxidasesNG-Nitroarginine Methyl EsterNitric OxideNitroprussideOxidative StressPhenylephrineAcetylcholineCyclooxygenase 2Cyclooxygenase 2 InhibitorsFree RadicalsMercuryNADPH OxidasesNG-Nitroarginine Methyl EsterNitric OxideNitroprussidePhenylephrineReactive Oxygen SpeciesSuperoxide DismutaseVasoconstrictor AgentsVasodilator Agents

Identifiers

PMID23145049
PMCPMC3492199
OpenAlexW1996326547

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.