Evidence map›Paper›PMID 21494558›Full record

ArticlePloS one2011

Acute lead exposure increases arterial pressure: role of the renin-angiotensin system.

Maylla Ronacher Simões, Eduardo Hertel Ribeiro, Marcos Vinícius A Vescovi, Honério C de Jesus, Alessandra S Padilha, Ivanita Stefanon, Dalton V Vassallo, Mercedes Salaices, Mirian Fioresi

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
2.8field-weighted citation impact, top 12% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 77 citations in OpenAlex.

  1. Pooled it
  2. Metals, cardiovascular risk, and the interplay with oxidative stress: a mini-review.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Review
  3. Article
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  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Key Characteristics of Cardiovascular Toxicants.Environmental health perspectives · 2021
    Article
  11. Lead (Pb) exposure and heart failure risk.Environmental science and pollution research international · 2021
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. 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

9 authors at 3 institutions in 2 countries.

Maylla Ronacher SimõesPhysiological Sciences Post-Graduation Program, Federal University of Espírito Santo, Vitoria, Espírito Santo, Brazil.
Eduardo Hertel Ribeiro
Marcos Vinícius A Vescovi
Honério C de Jesus
Alessandra S Padilha
Ivanita Stefanon
Dalton V Vassallo
Mercedes Salaices
Mirian Fioresi
Universidade Federal do Espírito Santo · BREscola Superior de Ciências da Santa Casa de Misericórdia de Vitória · BRUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundChronic lead exposure causes hypertension and cardiovascular disease. Our purpose was to evaluate the effects of acute exposure to lead on arterial pressure and elucidate the early mechanisms involved in the development of lead-induced hypertension. METHODOLOGY/PRINCIPAL

findingsWistar rats were treated with lead acetate (i.v. bolus dose of 320 µg/Kg), and systolic arterial pressure, diastolic arterial pressure and heart rate were measured during 120 min. An increase in arterial pressure was found, and potential roles of the renin-angiotensin system, Na(+),K(+)-ATPase and the autonomic reflexes in this change in the increase of arterial pressure found were evaluated. In anesthetized rats, lead exposure: 1) produced blood lead levels of 37±1.7 µg/dL, which is below the reference blood concentration (60 µg/dL); 2) increased systolic arterial pressure (Ct: 109±3 mmHg vs Pb: 120±4 mmHg); 3) increased ACE activity (27% compared to Ct) and Na(+),K(+)-ATPase activity (125% compared to Ct); and 4) did not change the protein expression of the α1-subunit of Na(+),K(+)-ATPase, AT(1) and AT(2). Pre-treatment with an AT(1) receptor blocker (losartan, 10 mg/Kg) or an ACE inhibitor (enalapril, 5 mg/Kg) blocked the lead-induced increase of arterial pressure. However, a ganglionic blockade (hexamethonium, 20 mg/Kg) did not prevent lead's hypertensive effect.

conclusionAcute exposure to lead below the reference blood concentration increases systolic arterial pressure by increasing angiotensin II levels due to ACE activation. These findings offer further evidence that acute exposure to lead can trigger early mechanisms of hypertension development and might be an environmental risk factor for cardiovascular disease.

Indexed as

AnimalsArteriesAutonomic Nervous SystemBlood PressureEnvironmental ExposureHemodynamicsHypertensionLeadMalePeptidyl-Dipeptidase ARatsRats, WistarReflexRenin-Angiotensin SystemSodium-Potassium-Exchanging ATPaseLeadPeptidyl-Dipeptidase ASodium-Potassium-Exchanging ATPase

Identifiers

PMID21494558
PMCPMC3073979
OpenAlexW2008453452

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.