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Thèse de Doctorat
DOI
10.11606/T.42.2010.tde-25032010-142756
Document
Auteur
Nom complet
Maria Alicia Carrillo Sepulveda
Unité de l'USP
Domain de Connaissance
Date de Soutenance
Editeur
São Paulo, 2010
Directeur
Jury
Chaves, Maria Luiza Morais Barreto de (Président)
Carvalho, Hernandes Faustino de
Carvalho, Maria Helena Catelli de
Laurindo, Francisco Rafael Martins
Rossoni, Luciana Venturini
Titre en portugais
Participação do receptor AT2 da angiotensina II no relaxamento vascular promovido pelo hormônio tiroideano
Mots-clés en portugais
Célula muscular lisa vascular
Hormônios tiroideanos
Óxido Nítrico
Receptor AT2 da Angiotensina II
Sistema renina argiotensina
Vasodilatação
Resumé en portugais
A vasodilatação promovida pela triiodotironina (T3) ocorre por sua ação direta sobre o relaxamento das células musculares lisas vasculares (CMLV), porém os mecanismos envolvidos são desconhecidos. Neste estudo mostramos que o T3 rapidamente relaxa as CMLV através da geração de óxido nítrico (NO), via óxido nítrico sintase neuronal e induzível (nNOS e iNOS), efeitos mediados pela sinalização PI3K/Akt. Ensaios funcionais em aortas sem endotélio, incubados com T3, mostraram menor resposta contrátil a Fenilefrina (FE), efeito este revertido pelo L-NAME, inibidor da NOS. Aortas de ratos hipertiroideos apresentaram aumento do receptor de Angiotensina II (AngII) do tipo 2 (AT2), acompanhado de diminuição de proteínas contráteis. In vitro o T3 diminui estas proteínas contráteis via AT2. Aortas sem endotélio dos ratos hipertiroideos apresentaram menor reatividade a AngII e maior relaxamento ao nitroprussiato de sódio (NPS), efeitos estes mediados via AT2. Por fim, observamos que o T3 é capaz de induzir produção de NO nas CMLV via PI3K/Akt, a qual é ativada pelo AT2
Titre en anglais
Thyroid hormone induces vascular relaxation via angiotensin II type 2 receptor (AT2)
Mots-clés en anglais
Angiotensin II type 2 receptor
Nitric oxide
Renin Angiotensin system
Thyroid hormone
Vascular smooth muscle cell
Vasodilation
Resumé en anglais
3,3',5-triiodo-l-thyronine (T3) has been shown to induce vasodilation by its direct effect on vascular smooth muscle cells (VSMC). However, the mechanism by which T3 causes VSMC relaxation is still unknown. Here, we have shown that T3 causes rapid relaxation of VSMC via increased NO production from inducible and neuronal nitric oxide synthase (NOS). We further showed that these effects were mediated by PI3K/Akt signaling pathway. Vascular reactivity studies showed that endothelium-denuded aortas treated with T3 had a decreased response to phenylephrine which was reserved by L-NAME, NOS inhibitors. Aortas from hyperthyroid rats showed an upregulation of AT2 accompanied by decreased of contractile proteins. In vitro we observed that T3 decreases contractile proteins via AT2. Furthermore, endothelium-denuded aortas from hyperthyroid rats showed a decreased response to angiotensinII and augmented relaxation to sodium nitroprusside (SNP) via AT2 participation. Our data also suggests that PI3K/Akt signaling pathway is involved in T3-induced NO production in VSMC via AT2.
 
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Date de Publication
2010-03-29
 
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