DEFAR - Departamento de Farmácia

URI permanente desta comunidadehttp://www.hml.repositorio.ufop.br/handle/123456789/530

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2007 - 20082

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Tem arquivos: SimAssunto: search.filters.subject.Nitric oxide

Resultados da Pesquisa

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    Tx2-6 toxin of the Phoneutria nigriventer spider potentiates rat erectile function.
    (2008) Nunes, Kenia Pedrosa; Gonçalves, Andrey Christian da Costa; Lanza, Luciana Franco; Côrtes, Steyner de França; Cordeiro, Marta do Nascimento; Michael, Richardson; Pimenta, Adriano Monteiro de Castro; Webb, Robert Clinton; Garcia, Maria Elena de Lima Perez
    The venom of the spider Phoneutria nigriventer contains several toxins that have bioactivity in mammals and insects. Accidents involving humans are characterized by various symptoms including penile erection. Here we investigated the action of Tx2-6, a toxin purified from the P. nigriventer spider venom that causes priapism in rats and mice. Erectile function was evaluated through changes in intracavernosal pressure/mean arterial pressure ratio (ICP/MAP) during electrical stimulation of the major pelvic ganglion (MPG) of normotensive and deoxycorticosterone-acetate (DOCA)-salt hypertensive rats. Nitric oxide (NO) release was detected in cavernosum slices with fluorescent dye (DAF-FM) and confocal microscopy. The effect of Tx2-6 was also characterized after intracavernosal injection of a non-selective nitric oxide synthase (NOS) inhibitor, L-NAME. Subcutaneous or intravenous injection of Tx2-6 potentiated the elevation of ICP/MAP induced by ganglionic stimulation. L-NAME inhibited penile erection and treatment with Tx2-6 was unable to reverse this inhibition. Tx2-6 treatment induced a significant increase of NO release in cavernosum tissue. Attenuated erectile function of DOCA-salt hypertensive rats was fully restored after toxin injection. Tx2-6 enhanced erectile function in normotensive and DOCA-salt hypertensive rats, via the NO pathway. Our studies suggest that Tx2-6 could be important for development of new pharmacological agents for treatment of erectile dysfunction.
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    Endothelium-dependent vasodilation induced by Hancornia speciosa in rat superior mesenteric artery.
    (2007) Ferreira, Herick Campos; Serra, Carla Penido; Endringer, Denise Coutinho; Lemos, Virgínia Soares; Braga, Fernão Castro; Côrtes, Steyner de França
    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.