Acute lead exposure increases arterial pressure: Role of the renin-angiotensin system
| Autor: | Rogério Faustino Ribeiro Júnior, Dalton Valentim Vassallo, Mirian Fioresi, Honério Coutinho de Jesus, Maylla Ronacher Simões, Alessandra Simão Padilha, Mercedes Salaices, Ivanita Stefanon, Marcos Vinícius A. Vescovi |
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| Přispěvatelé: | UAM. Departamento de Farmacología |
| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Male
Anatomy and Physiology Hemodynamics lcsh:Medicine Blood Pressure Heavy Metals Cardiovascular Cardiovascular System Renin-Angiotensin System Medicine lcsh:Science Multidisciplinary Environmental exposure Animal Models Arteries Chemistry Losartan Hypertension Cardiology Circulatory Physiology Sodium-Potassium-Exchanging ATPase medicine.drug Research Article medicine.medical_specialty Pollutants Medicina Peptidyl-Dipeptidase A Autonomic Nervous System Model Organisms Internal medicine Renin–angiotensin system Reflex Environmental Chemistry Animals Rats Wistar Biology business.industry lcsh:R Environmental Exposure Angiotensin II Surgery Rats Blood pressure Lead Lead acetate ACE inhibitor Cardiovascular Anatomy Rat lcsh:Q business |
| Zdroj: | PLoS ONE, Vol 6, Iss 4, p e18730 (2011) PLoS ONE Biblos-e Archivo. Repositorio Institucional de la UAM instname |
| ISSN: | 3976-7531 |
| Popis: | 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 This 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 |
| Databáze: | OpenAIRE |
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