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Vasorelaxant Effect of Osterici Radix Ethanol Extract on Rat Aortic Rings

The root of Ostericum koreanum Maximowicz has been used as a traditional medicine called “Kanghwal” in Korea (or “Qianghuo” in China). The purpose of this study was to investigate the vasorelaxant activity and mechanism of action of an ethanol extract of the O. koreanum root (EOK). We used isolated...

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Detalles Bibliográficos
Autores principales: Lee, Kyungjin, Park, Geunyong, Ham, Inhye, Yang, Gabsik, Lee, Mihwa, Bu, Youngmin, Kim, Hocheol, Choi, Ho-Young
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3800564/
https://www.ncbi.nlm.nih.gov/pubmed/24204390
http://dx.doi.org/10.1155/2013/350964
Descripción
Sumario:The root of Ostericum koreanum Maximowicz has been used as a traditional medicine called “Kanghwal” in Korea (or “Qianghuo” in China). The purpose of this study was to investigate the vasorelaxant activity and mechanism of action of an ethanol extract of the O. koreanum root (EOK). We used isolated rat aortic rings to assess the effects of EOK on various vasorelaxant or vasoconstriction factors. EOK induced vasorelaxation in phenylephrine hydrochloride (PE) or KCl precontracted aortic rings in a concentration-dependent manner. However, the vasorelaxant effects of EOK on endothelium-intact aortic rings were reduced by pretreatment with L-NAME or methylene blue. In Ca(2+)-free Krebs-Henseleit solution, pretreatment with EOK (0.3 mg/mL) completely inhibited PE-induced constriction. In addition, EOK (0.3 mg/mL) also completely inhibited vasoconstriction induced by supplemental Ca(2+) in aortic rings that were precontracted with PE or KCl. Furthermore, the EOK-induced vasorelaxation in PE-contracted aortic rings was inhibited by preincubation with nifedipine. These results indicate that the vasorelaxant effects of EOK are responsible for the induction of NO formation from L-Arg and NO-cGMP pathways, blockage of the extracellular Ca(2+) entry via the receptor-operative Ca(2+) channel and voltage-dependent calcium channel, and blockage of sarcoplasmic reticulum Ca(2+) release via the inositol triphosphate pathway.