Ação vasodilatadora de inositóis
Ano de defesa: | 2015 |
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Autor(a) principal: | |
Orientador(a): | |
Banca de defesa: | |
Tipo de documento: | Tese |
Tipo de acesso: | Acesso aberto |
Idioma: | por |
Instituição de defesa: |
Universidade Federal de Minas Gerais
UFMG |
Programa de Pós-Graduação: |
Não Informado pela instituição
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Departamento: |
Não Informado pela instituição
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País: |
Não Informado pela instituição
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Palavras-chave em Português: | |
Link de acesso: | http://hdl.handle.net/1843/BUBD-AB6FP9 |
Resumo: | Inositols are natural compounds from animal and plant sources present in human diet. They have an important role in cell metabolism and they are used in the treatment of metabolic illnesses. Recent studies suggest that inositols have a protective effect on the cardiovascular system, characterized by the reductionof the endothelium dysfunction. The precise mechanism of this protective effect is unknown, but could be related to their antioxidant and metabolic effects. The work aimed at investigating the direct vasodilator effect and respective mechanism of action of myo-inositol, chiro-inositol and bornesitol in rat aorta. The inositols induced a concentration- and endothelium-dependent vasodilation, abolished by a non-selective inhibitor of nitric oxide synthase (NOS). Fluorescent analysis with DAF-2, a selective dye for nitric oxide (NO), demonstrated that the inositols increased the production of NO. Western blot data demonstrated that the inositols increased the phosphorylation level of the activation site of the endothelial NOS (eNOS). Selective inhibitors of phosphatidylinositol-3 kinase (PI-3K) did not change the vasodilator effect of the inositols. However, the selective inhibition of calmodulin significantly reduced the vasodilation induced inositols. Also, the inositols increased the intracellular concentration of calcium in the endothelium of rat aortic rings. The present results allow concluding that myo-inositol, chiro-inositol and bornesitol induce an endothelium- and NO-dependent direct vasodilator effect, through the activation of eNOS by a calcium-dependent mechanism of action. |