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Evidence-Based Complementary and Alternative Medicine
Volume 2013, Article ID 350964, 8 pages
http://dx.doi.org/10.1155/2013/350964
Research Article

Vasorelaxant Effect of Osterici Radix Ethanol Extract on Rat Aortic Rings

Department of Herbology, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 130-701, Republic of Korea

Received 5 April 2013; Revised 17 August 2013; Accepted 19 August 2013

Academic Editor: Bo-Hyoung Jang

Copyright © 2013 Kyungjin Lee et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

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 Ca2+-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 Ca2+ 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 Ca2+ entry via the receptor-operative Ca2+ channel and voltage-dependent calcium channel, and blockage of sarcoplasmic reticulum Ca2+ release via the inositol triphosphate pathway.