Low-level lead exposure increases systolic arterial pressure and endothelium-derived vasodilator factors in rat aortas
| Autor: | Rogério Faustino Ribeiro Júnior, Alessandra Simão Padilha, Edna Aparecida Silveira, Honério Coutinho de Jesus, Dalton Valentim Vassallo, Mercedes Salaices, Marcos Vinícius A. Vescovi, Ivanita Stefanon, Jonaina Fiorim |
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| Přispěvatelé: | UAM. Departamento de Farmacología |
| Jazyk: | angličtina |
| Rok vydání: | 2011 |
| Předmět: |
Male
medicine.medical_specialty Endothelium Medicina Toxic Agents Aortic Diseases lcsh:Medicine Blood Pressure Cardiovascular Toxicology Cardiovascular Pharmacology Nitric oxide Renin-Angiotensin System chemistry.chemical_compound Vascular Biology Internal medicine medicine Animals Rats Wistar lcsh:Science Phenylephrine Aorta Endothelium-Dependent Relaxing Factors Multidisciplinary Dose-Response Relationship Drug biology lcsh:R Rats Nitric oxide synthase Lead Poisoning Dose–response relationship Endocrinology medicine.anatomical_structure Losartan Lead chemistry Vasoconstriction Hypertension biology.protein Medicine lcsh:Q Sodium nitroprusside Endothelium Vascular Sodium-Potassium-Exchanging ATPase medicine.symptom Research Article medicine.drug |
| Zdroj: | PLoS ONE, Vol 6, Iss 2, p e17117 (2011) Biblos-e Archivo. Repositorio Institucional de la UAM instname PLoS ONE |
| ISSN: | 1932-6203 3976-7531 |
| Popis: | Chronic lead exposure induces hypertension and alters endothelial function. However, treatment with low lead concentrations was not yet explored. We analyzed the effects of 7 day exposure to low lead concentrations on endothelium-dependent responses. Wistar rats were treated with lead (1st dose 4 μg/100 g, subsequent dose 0.05 μg/100 g, i.m. to cover daily loss) or vehicle; blood levels attained at the end of treatment were 9.98 μg/dL. Lead treatment had the following effects: increase in systolic blood pressure (SBP); reduction of contractile response to phenylephrine (1 nM-100 μM) of aortic rings; unaffected relaxation induced by acetylcholine (0.1 nM-300 μM) or sodium nitroprusside (0.01 nM-0.3 μM). Endothelium removal, NG-nitro-L-arginine methyl ester (100 μM) and tetraethylammonium (2 mM) increased the response to phenylephrine in treated rats more than in untreated rats. Aminoguanidine (50 μM) increased but losartan (10 μM) and enalapril (10 μM) reduced the response to phenylephrine in treated rats. Lead treatment also increased aortic Na+/K+-ATPase functional activity, plasma angiotensin-converting enzyme (ACE) activity, protein expression of the Na+/K+-ATPase alpha-1 subunit, phosphorylated endothelial nitric oxide synthase (p-eNOS), and inducible nitric oxide synthase (iNOS). Our results suggest that on initial stages of lead exposure, increased SBP is caused by the increase in plasma ACE activity. This effect is accompanied by increased p-eNOS, iNOS protein expression and Na+/K+-ATPase functional activity. These factors might be a compensatory mechanism to the increase in SBP This study was supported by grants from CAPES (Coordenação de Aperfeiçoamento Pessoal de Nível Superior) and CNPq (Conselho Nacional de desenvolvimento Científico e Tecnológico)/FAPES (Fundação de Apoio à Pesquisa do Espírito Santo)/FUNCITEC (Fundação de Ciência e Tecnologia) (39767531/07), Brazil and from MCINN (SAF 2009-07201) and ISCIII (Red RECAVA, RD06/0014/0011), Spain |
| Databáze: | OpenAIRE |
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