Vasorelaxant effect of osterici radix ethanol extract on rat aortic rings.

Evid Based Complement Alternat Med

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

Published: November 2013

AI Article Synopsis

  • The root of Ostericum koreanum, known for its traditional medicinal use in Korea and China, was examined for its ability to promote vasorelaxation.
  • The ethanol extract of O. koreanum (EOK) showed concentration-dependent vasorelaxant effects on aortic rings, but its effectiveness decreased when certain inhibitors were applied.
  • The study suggests that EOK's vasorelaxation occurs through mechanisms involving nitric oxide (NO) production, blockage of calcium entry, and inhibition of calcium release from the sarcoplasmic reticulum.

Article 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 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.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3800564PMC
http://dx.doi.org/10.1155/2013/350964DOI Listing

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