Acute lead exposure increases arterial pressure: Role of the renin-angiotensin system
EntityUAM. Departamento de Farmacología
PublisherPublic Library of Science
10.1371/journal.pone.0018730Plos One 6.4 (2011): e18730
Funded byThis study was supported by grants from CAPES (Coordenação de Aperfeiçoamento de Pessoal de Nível Superior) and CNPq (Conselho Nacional de Desenvolvimento Científico e Tecnológico)/FAPES (Fundação de Amparo à Pesquisa do Espírito Santo)/FUNCITEC (Fundação de Ciência e Tecnologia)(39767531/07), Brazil and from MCINN (Ministerio de Ciencia e Innovación) (SAF 2009- 07201) and ISCIII (Instituto de Salud Carlos III) (Red RECAVA- Red Temática de Investigación en Enfermedades Cardiovasculares del Instituto de Salud Carlos III, RD06/0014/0011), Spain
SubjectsAutonomic Nervous System; Environmental Exposure; Hypertension; Peptidyl-Dipeptidase A; Reflex; Medicina
Rights© 2011 Simões et al.
Esta obra está bajo una Licencia Creative Commons Atribución 4.0 Internacional.
Background: Chronic 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 Findings: Wistar 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, AT1 and AT2. Pre-treatment with an AT1 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. Conclusion: Acute 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
Google Scholar:Simões, Maylla Ronacher - Ribeiro, Rogério Faustino - Vescovi, Marcos Vinícius Altoé - De Jesus, Honério Coutinho - Padilha, Alessandra Simão - Stefanon, Ivanita - Vassallo, Dalton Valentim - Salaices Sánchez, Mercedes - Fioresi, Mirian
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Fernandes Azevedo, Bruna; Barros Furieri, Lorena; Peçanha, Franck MacIel; Wiggers, Giulia Alessandra; Frizera Vassallo, Paula; Ronacher Simões, Maylla; Fiorim, Jonaína; Rossi de Batista, Priscila; Fioresi, Mirian; Rossoni, Luciana Venturini; Stefanon, Ivanita; Alonso, María Jesús; Salaices Sánchez, Mercedes; Valentim Vassallo, Dalton