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Evaluation of the mechanisms involved on the endothelium-dependent vasodilation in aorta of isoproterenol-treated mice

Grant number: 11/16017-4
Support type:Scholarships in Brazil - Master
Effective date (Start): March 01, 2012
Effective date (End): June 30, 2013
Field of knowledge:Biological Sciences - Physiology
Principal researcher:Luciana Venturini Rossoni
Grantee:Angelo Bernak de Oliveira
Home Institution: Instituto de Ciências Biomédicas (ICB). Universidade de São Paulo (USP). São Paulo , SP, Brazil

Abstract

The acute stimulation of beta-adrenoceptors (beta-AR) on the vessels induces vasodilatation through the activation of protein kinase A (PKA) and/ or synthesis and release of nitric oxide (NO). Microdomains in the plasma membrane of endothelial cells enriched in colesterol and caveolin (cav)-1, the caveolae, modulates the nitric oxide synthase (NOS) activity as well as the beta-AR activity. Previous results demonstrated that aorta from beta1-AR knockout (beta1-KO) mice showed an impairment of endothelium-dependent relaxation induced by acetylcholine (ACh), without changes on endothelium-independent relaxation to NO donor, suggesting that this artery has endothelial dysfunction. It is well known that chronic stimulation of beta-AR is associated with cardiac hypertrophy, and the treatment with non-selective beta-AR agonist, isoproterenol (ISO), induces this effect. Previous results in aorta from 7-days ISO-treated rat and mice demonstrated an exacerbated phenylephrine-induced contraction, oxidative stress and synthesis of pro-inflammatory cytokines, as well as the enhanced protein expression of endothelial and neuronal NOS (eNOS and nNOS, respectively) and cav-1, without changes in ACh-induced relaxation. These results suggested that cav-1 modulates eNOS activity. However, there are no functional studies that demonstrated this modulation as well as the beta-AR involved in this response. Moreover, the ISO-treatment improved the impaired ACh-induced relaxation observed in aorta beta1-KO mice. Taken together, these results suggested the hypothesis of the interaction among caveolae, NO synthesis and beta1-AR is associated with the effects induced by ISO treatment. Thus, the present project aim to investigate: 1) the mechanisms associated with the endothelial dysfunction observed in aorta of beta1-KO mice; and 2) the role of caveolae on the ACh-induced relaxation observed in aorta from ISO-treated mice, focusing on the role of beta1-AR.

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Scientific publications
(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
BERNAK-OLIVEIRA, ANGELO; GUIZONI, DANIELE M.; CHIAVEGATTO, SILVANA; DAVEL, ANA P.; V. ROSSONI, LUCIANA. The protective role of neuronal nitric oxide synthase in endothelial vasodilation in chronic beta-adrenoceptor overstimulation. Life Sciences, v. 285, . (10/50048-1, 11/16017-4, 17/06100-8)
Academic Publications
(References retrieved automatically from State of São Paulo Research Institutions)
OLIVEIRA, Angelo Bernak de. Evaluation of the mechanisms involved on the endothelium-dependent vasodilation in aorta of isoproterenol-treated mice.. 2014. Master's Dissertation - Universidade de São Paulo (USP). Instituto de Ciências Biomédicas (ICB/SDI) São Paulo.

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