Avaliação pré-clínica dos efeitos cardiovasculares induzidos pelo liofilizado do vinho tinto do Vale do Rio São Francisco em ratos abordagem in vivo e in vitro

• Autor(a) principal: Oliveira, Aurylene Carlos de
• Data de Publicação: 2011
• Tipo de documento: Tese
• Idioma: por
• Título da fonte: Biblioteca Digital de Teses e Dissertações da UFPB
• Texto Completo: https://repositorio.ufpb.br/jspui/handle/tede/6716
• topic: Vinho tinto; Hipotensão; Vasorelaxamento; Óxido nítrico; Red wine; Hypotension; Vasorelaxation; Nitric oxide; CIENCIAS BIOLOGICAS::FARMACOLOGIA

Several epidemiological studies indicated that regular intake of red wine is associated with a decrease global mortality. The protective effect has been attributable, at least in part, to polyphenols. The cardiovascular effects induced by lyophilized red wine from Vale do São Francisco (LVTVSF) were evaluated in this study using in vivo and in vitro assays. The lyophilized red wine from Vale do São Francisco (LVTVSF) contains a series of flavonols, such, quercetin, myricetin and kaempferol. The red wine lyophilized was able to reduce mean arterial pressure (MAP) in L-NAME hypertensive rats compared to controls (143.7 ± 4.7 versus 172.5 ± 4.7 mmHg). In normotensive rats the administration of LVTVSF (10, 30, 90 mg/kg i.v.) randomly, induced hypotension (-24.0 ± 1.2; -32.4 ± 1.3; -51.4 ± 1.5%) and tachycardic effects (14.5 ± 2.3; 19.5 ± 1.7; 28.4 ± 2.1%). The pre-treatment with L-NAME (20 mg / kg i.v.), inhibitor of endothelial nitric oxide synthase, attenuated the hypotensive effect induced by LVTVSF. In isolated normotensive rat mesenteric artery rings LVTVSF elicited concentration-dependent relaxation of PHE-induced contraction (MR = 87.22 ± 3.59%). After removal of the vascular endothelial the vasorelaxant effect was significantly attenuated (MR = 32.07 ± 2.07%, p < 0.05), suggesting the involvement of endothelium-derived relaxing factor. After incubation with L-NAME (100 μM) and ODQ (10 mM), inhibitor of soluble guanylyl cyclase, the relaxation response was significantly attenuated (MR= 22.64 ± 3.74%, p < 0.05; MR = 37.08 ± 4.60%, p < 0.05, respectively). Similar results was also obtained rings incubed with KCl (20 mM), a modulator of potassium efflux; TEA (1 mM), nonselective blocker for potassium channels; (MR = 46.04 ± 9.87%, p < 0,05; MR = 44.40 ± 5.80%, p < 0,05; respectively). The LVTVSF was able to increase the NO levels in endothelial cells of the rabbit aorta. In the presence of charybdotoxin and apamin the relaxant response was not attenuated. Incubation with inhibitors of reactive oxygen species, N-acetylcysteine (NAC) (10 mM), tempol (100 μM) and apocynin (10 μM), reduces the vasorelaxation. After pre-treatment with atropine and indometacin, the vasorelaxant effect induced by LVTVSF was no attenuated. In endothelial cells of the rabbit aorta LVTVSF was able to increase production of ROS. These results together suggest that the hypotensive effect induced by LVTVSF in normotensive rats is probably due to a decrease in total peripheral resistance as a result of activation of the eNOS-NO-cGMP, involving the redox sensitive mechanism. These effects may be due to flavonoids found in LVTVSF.