4.2 Article

Vasorelaxant effect of Prunus yedoensis bark

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BMC
DOI: 10.1186/1472-6882-13-31

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Funding

  1. Korea Healthcare technology R&D Project, Ministry of Health & Welfare, Republic of Korea [B110081]
  2. Korea Health Promotion Institute [B110081] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)

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Background: Prunus yedoensis Matsum. is used as traditional medicine-'Yaeng-Pi' or 'Hua-Pi'-in Japan and Korea. However, no studies have examined the pharmacological activities of the P. yedoensis bark. Only the antioxidant and antiviral activities of P. yedoensis fruit and the anti-hyperglycaemic effect of P. yedoensis leaf have been investigated. While studying the antihypertensive effects of several medicinal plants, we found that a methanol extract of P. yedoensis bark (MEPY) had distinct vasorelaxant effects on rat aortic rings. Methods: The aortic rings were removed from Sprague-Dawley rats and suspended in organ chambers containing 10 ml Krebs-Henseleit solution. The aortic rings were placed between 2 tungsten stirrups and connected to an isometric force transducer. Changes in tension were recorded via isometric transducers connected to a data acquisition system. Results: MEPY relaxed the contraction induced by phenylephrine (PE) both in endothelium-intact and endothelium-denuded aortic rings concentration dependently. However, the vasorelaxant effects of MEPY on endothelium-denuded aortic rings were lower than endothelium-intact aortic rings. The vasorelaxant effects of MEPY on endothelium-intact aortic rings were reduced by pre-treatment with L-NAME, methylene blue, or ODQ. However, pre-treatment with indomethacin, atropine, glibenclamide, tetraethylammonium, or 4-aminopyridine had no affection. In addition, MEPY inhibited the contraction induced by extracellular Ca2+ in endothelium-denuded rat thoracic aorta rings pre-contracted by PE (1 mu M) or KCl (60 mM) in Ca2+-free solution. Conclusions: Our results suggest that MEPY exerts its vasorelaxant effects via the activation of NO formation by means of L-Arg and NO-cGMP pathways and via the blockage of extracellular Ca2+ channels.

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