title: Reactive oxygen and nitrogen species balance in the determination of thyroid hormones-induced cardiac hypertrophy mediated by renin-angiotensin system.
abstract: Role of reactive oxygen species (ROS)/nitric oxide (NO) balance and renin-angiotensin system in mediating cardiac hypertrophy in hyperthyroidism was evaluated in an in vivo and in vitro experimental model. Male Wistar rats were divided into four groups: control, thyroid hormone, vitamin E (or Trolox, its hydrosoluble analogue), thyroid hormone+vitamin E. Angiotensin II receptor (AT1/AT2) gene expression, immunocontent of AT1/AT2 receptors, angiotensinogen, NADPH oxidase (Nox2), and nitric oxide synthase isoforms, as well as ROS concentration (hydrogen peroxide and superoxide anion) were quantified in myocardium. Thyroid hormone increased ROS and NO metabolites, iNOS, nNOS and eNOS isoforms and it was accompanied by cardiac hypertrophy. AT1/AT2 expression and the immunocontent of angiotensinogen and Nox2 were enhanced by thyroid hormone. Antioxidants reduced ROS levels, Nox2, AT1/AT2, NOS isoforms and cardiac hypertrophy. In conclusion, ROS/NO balance may play a role in the control of thyroid hormone-induced cardiac hypertrophy mediated by renin-angiotensin system.
authors.affiliation: Departamento de Fisiologia, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
authors.forename: A S R
authors.initials: AS
authors.lastname: Araujo
authors.forename: G P
authors.initials: GP
authors.lastname: Diniz
authors.forename: F E R
authors.initials: FE
authors.lastname: Seibel
authors.forename: G
authors.initials: G
authors.lastname: Branchini
authors.forename: M F M
authors.initials: MF
authors.lastname: Ribeiro
authors.forename: I S
authors.initials: IS
authors.lastname: Brum
authors.forename: N
authors.initials: N
authors.lastname: Khaper
authors.forename: M L M
authors.initials: ML
authors.lastname: Barreto-Chaves
authors.forename: A
authors.initials: A
authors.lastname: Belló-Klein
mesh_terms: D000808:Angiotensinogen / Q000032:analysis; D000818:Animals; D015153:Blotting, Western; D006332:Cardiomegaly / Q000378:metabolism / Q000473:pathology*; D002478:Cells, Cultured; D002839:Chromans / Q000494:pharmacology; D006980:Hyperthyroidism / Q000378:metabolism; D008297:Male; D019255:NADPH Oxidases / Q000032:analysis; D009569:Nitric Oxide / Q000032:analysis; D019001:Nitric Oxide Synthase / Q000235:genetics; D016133:Polymerase Chain Reaction; D051381:Rats; D017208:Rats, Wistar; D026361:Reactive Nitrogen Species / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*; D044140:Receptor, Angiotensin, Type 1 / Q000235:genetics / Q000378:metabolism; D044139:Receptor, Angiotensin, Type 2 / Q000235:genetics / Q000378:metabolism; D011945:Receptors, Angiotensin / Q000235:genetics; D012084:Renin-Angiotensin System / Q000502:physiology*; D013963:Thyroid Hormones / Q000378:metabolism* / Q000494:pharmacology; D014810:Vitamin E / Q000494:pharmacology
chemical_list: D002839:Chromans; D026361:Reactive Nitrogen Species; D017382:Reactive Oxygen Species; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D013963:Thyroid Hormones; D000808:Angiotensinogen; D014810:Vitamin E; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase; D019255:NADPH Oxidases; C010643:6-hydroxy-2,5,7,8-tetramethylchroman-2-carboxylic acid