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ORIGINAL ARTICLE
Year : 2019  |  Volume : 15  |  Issue : 60  |  Page : 59-65

Vasorelaxant effect of the ethanol extract from Valeriana fauriei briquet root and rhizome on rat thoracic aorta


1 Department of Herbology, College of Korean Medicine, Seoul 02447, Republic of Korea
2 Graduate School, Kyung Hee University, Seoul 02447, Republic of Korea
3 Department of Biomedical Science and Technology, Kyung Hee University, Seoul 02447, Republic of Korea

Correspondence Address:
Ho-Young Choi
Department of Herbology, College of Korean Medicine, Kyung Hee University, 26 Kyungheedae-ro, Dongdaemun-gu, Seoul 02447
Republic of Korea
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/pm.pm_152_18

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Background: Valeriana fauriei has been used to treat anxiety and cardiovascular disease in many countries; however, the mechanisms of the vasorelaxant effect of V. fauriei roots and rhizomes have not been elucidated. Purpose of the Study: Considering the increased use of traditional medicines for treating hypertension, the aim of this study was to examine the vasorelaxant effect and investigate the mechanisms of V. fauriei root and rhizome. Materials and Methods: Using an isolated organ-chamber technique, the vasorelaxant effects of 70% ethanol extract of V. fauriei root and rhizome (VFE) were tested in rat aortic ring segments. Results: VFE concentration dependently relaxed both endothelium-intact and endothelium-denuded aortic rings that were precontracted by phenylephrine (PE) or potassium chloride (KCl). VFE relaxed the aortic rings precontracted by PE (1 μM) irrespective of K+ channel blocker pretreatment such as tetraethylammonium, glibenclamide, or 4-aminopyridine. VFE inhibited vasoconstriction caused by extracellular Ca2+ influx through receptor-operative Ca2+ channels (ROCCs) or voltage-dependent Ca2+ channels (VDCCs) activated by PE or KCl, respectively, in Ca2+-free Krebs–Henseleit buffer. Conclusion: These results suggested that the vasorelaxant effects of VFE were endothelium independent and not related to K+ channels, such as Ca2+-activated K+ channels, ATP-sensitive K+ channels, and Voltage-gated K+ channels. In addition, VFE relaxed the aortic rings by blocking the influx of extracellular Ca2+ through ROCCs and VDCCs. Abbreviations used: ACE: Angiotensin-converting enzyme; VFE: The 70% EtOH extract of Valeriana fauriei root and rhizome; KH: Krebs–Henseleit; PE: Phenylephrine; KCl: Potassium chloride; TEA: Tetraethylammonium; 4-AP: 4-Aminopyridine; CaCl2: Calcium chloride; EGTA: Ethylene glycol-bis (2-aminoethylether)-N, N, N′, N′-tetraacetic acid; DMSO: Dimethyl sulfoxide; ROCCs: Receptor-operative Ca2+ channels; VDCCs: Voltage-dependent Ca2+ channels; KIR: Inward-rectifier K+ channels; KATP: ATP-sensitive K+ channels; KV: Voltage-gated K+ channels; KCa: Ca2+-activated K+ channels.


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