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Endothelium-Independent Vasorelaxant Effects of Hydroalcoholic Extract from Nigella sativa Seed in Rat Aorta: The Roles of Ca(2+) and K(+) Channels

Objective. The aim of this study was to elucidate the mechanism(s) responsible for the vasorelaxant effect of Nigella sativa (N. sativa). Methods. The activity of different concentrations of N. sativa extract was evaluated on contractile responses of isolated aorta to KCl and phenylephrine (PE). Res...

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Detalles Bibliográficos
Autores principales: Niazmand, Saeed, Fereidouni, Elahe, Mahmoudabady, Maryam, Mousavi, Seyed Mojtaba
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4036417/
https://www.ncbi.nlm.nih.gov/pubmed/24900958
http://dx.doi.org/10.1155/2014/247054
Descripción
Sumario:Objective. The aim of this study was to elucidate the mechanism(s) responsible for the vasorelaxant effect of Nigella sativa (N. sativa). Methods. The activity of different concentrations of N. sativa extract was evaluated on contractile responses of isolated aorta to KCl and phenylephrine (PE). Results. The extract (2–14 mg/mL) induced a concentration dependent relaxation both in endothelium-intact and endothelium-denuded aortic rings precontracted by PE (10(−6) M) and KCl (6 × 10(−2) M). Extract reduced PE- and KCl-induced contractions in presence of cumulative concentrations of calcium (10(−5)–10(−2) M) significantly. L-NAME and indomethacin had no effect on vasorelaxation effect of extract in PE-induced contraction. Diltiazem and heparin reduced significantly this vasorelaxation at a concentration of 14 mg/mL of extract; however, N. sativa-induced relaxation was not affected by ruthenium red. Tetraethylammonium chloride reduced the extract-induced relaxation in concentrations of 2–6 mg/mL of extract significantly but glibenclamide reduced this relaxative effect in all concentrations of extract. Conclusions. The inhibitory effect of N. sativa seed extract on the contraction induced by PE and KCl was endothelium-independent. This relaxation was mediated mainly through the inhibition of Ca(2+) and K(ATP) channels and also intracellular calcium release.