Simvastatin prevents load-induced protein tyrosine nitration in overloaded hearts

dc.creatorNadruz, W
dc.creatorLagosta, VJ
dc.creatorMoreno, H
dc.creatorCoelho, OR
dc.creatorFranchini, KG
dc.date2004
dc.dateMAY
dc.date2014-11-18T13:38:54Z
dc.date2015-11-26T16:27:50Z
dc.date2014-11-18T13:38:54Z
dc.date2015-11-26T16:27:50Z
dc.date.accessioned2018-03-28T23:08:48Z
dc.date.available2018-03-28T23:08:48Z
dc.identifierHypertension. Lippincott Williams & Wilkins, v. 43, n. 5, n. 1060, n. 1066, 2004.
dc.identifier0194-911X
dc.identifierWOS:000221113200029
dc.identifier10.1161/01.HYP.0000124252.43470.2c
dc.identifierhttp://www.repositorio.unicamp.br/jspui/handle/REPOSIP/74248
dc.identifierhttp://www.repositorio.unicamp.br/handle/REPOSIP/74248
dc.identifierhttp://repositorio.unicamp.br/jspui/handle/REPOSIP/74248
dc.identifier.urihttp://repositorioslatinoamericanos.uchile.cl/handle/2250/1269298
dc.descriptionHydroxymethylglutaryl-coenzyme A reductase inhibitors prevent load-induced left ventricular hypertrophy (LVH). Whether this effect is related to antioxidant properties of this class of drugs is poorly understood. The aim of the present report was to evaluate the regulation of nitrotyrosine production during the development of load-induced LVH and the effect of simvastatin treatment in this process. Rats were subjected to aortic constriction up to 15 days. LVH was evaluated by left/right ventricle mass ratio. Myocardial content of nitrotyrosine, nitric oxide synthase ( NOS) isoforms, and phagocyte-type NAD(P)H-oxidase subunits (p67-phox and p22-phox) were analyzed by immunoblotting and immunohistochemistry assays. Another group of rats received treatment with either simvastatin or placebo for 15 days after the onset of pressure overload, and their hearts were also studied. Myocardial nitrotyrosine content was increased from 3 to 15 days of pressure overload in regions of cardiac myocytes in close apposition to myocardial stroma during LVH. Neuronal NOS ( nNOS), inducible NOS ( iNOS), and endothelial NOS ( eNOS) isoforms had their expression increased in coronary vessels ( nNOS and iNOS) and in myocardial stroma ( eNOS) from day 3 to day 7 of aortic constriction. However, p67-phox and p22-phox expression was increased in cells of myocardial stroma in parallel to augmented myocardial nitrotyrosine content. Simvastatin treatment inhibited the increases in myocardial nitrotyrosine content and in p67-phox and p22-phox expression, and significantly reduced LVH. In conclusion, antioxidant properties of simvastatin might play a role in myocardial remodeling induced by pressure overload.
dc.description43
dc.description5
dc.description1060
dc.description1066
dc.languageen
dc.publisherLippincott Williams & Wilkins
dc.publisherPhiladelphia
dc.publisherEUA
dc.relationHypertension
dc.relationHypertension
dc.rightsfechado
dc.sourceWeb of Science
dc.subjecthypertrophy
dc.subjectcardiac function
dc.subjectheart
dc.subjectoxidative stress
dc.subjectstatins
dc.subjectLeft-ventricular Hypertrophy
dc.subjectInduced Cardiac-hypertrophy
dc.subjectCoa Reductase Inhibitor
dc.subjectNitric-oxide Synthases
dc.subjectPressure-overload
dc.subjectAngiotensin-ii
dc.subjectNadph Oxidase
dc.subjectPeroxynitrite
dc.subjectSuperoxide
dc.subjectExpression
dc.titleSimvastatin prevents load-induced protein tyrosine nitration in overloaded hearts
dc.typeArtículos de revistas


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