Endothelium-dependent vasodilation induced by Hancornia speciosa in rat superior mesenteric artery.

• Autor(a) principal: Ferreira, Herick Campos
• Data de Publicação: 2007
• Outros Autores: Serra, Carla Penido, Endringer, Denise Coutinho, Lemos, Virgínia Soares, Braga, Fernão Castro, Côrtes, Steyner de França
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFOP
• Texto Completo: http://www.repositorio.ufop.br/handle/123456789/1213
• topic: Hancornia speciosa; Resistance artery; Vasodilation; Endothelium; Nitric oxide

The vasodilator effect of the ethanolic extract of leaves from Hancornia speciosa Gomes (HSE) was evaluated in superior mesenteric artery rings. HSE produced a concentration-dependent vasodilation (IC50 ¼ 10.874.0 mg/mL) in arterial rings pre-contracted with phenylephrine, which was completely abolished in endothelium-denuded vessels. Endothelium-dependent vasodilation induced by HSE was strongly reduced by L-NAME (100 mM), a nitric oxide (NO) synthase inhibitor, but neither by atropine, a muscarinic receptor antagonist (1 mM), nor by indomethacin (10 mM), a cyclooxygenase inhibitor. In rings pre-contracted with 80mM KCl, the vasodilator effect of HSE was shifted to the right and was completely abolished in the presence of L-NAME (100 mM). Similar effects were obtained in mesenteric rings pre-contracted with phenylephrine in the presence of KCl 25mM alone or in addition to 100 mM L-NAME.In addition, BaCl2 (1mM) dramatically reduced the vasodilation induced by HSE. Together, these findings led usv to conclude that HSE induces an endothelium-dependent vasodilation in rat mesenteric artery, by a mechanism dependent on NO, on the activation of potassium channels and endothelium-derived hyperpolarizing factor release. Rutin, identified as a major peak in the HPLC fingerprint obtained for HSE, might contribute for the observed vasodilator effect, since it was able to induce an endothelium-dependent vasodilation in rat superior mesenteric arteries.