alexa Cardio-Electopharmacology and Vasodilating Mechanisms of Quercetin
ISSN: 2161-0444

Medicinal Chemistry
Open Access

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Review Article

Cardio-Electopharmacology and Vasodilating Mechanisms of Quercetin

Hiroyasu Satoh* and Seiichiro Nishida

Health Life Science, Shitennoji University, Habikino, Osaka 583-8501, Japan

*Corresponding Author:
Dr. Hiroyasu Satoh
Health Life Science Shitennoji University
3-2-1 Gakuenmae, Habikino
Osaka 583-8501, Japan
Tel: +81-72-956- 3181
Fax: +81-72-956-6011
E-mail: [email protected]

Received date: April 29, 2014; Accepted date: June 25, 2014; Published date: June 27, 2014

Citation: Satoh H, Nishida S (2014) Cardio-Electopharmacology and Vasodilating Mechanisms of Quercetin. Med chem 4:523-530. doi:10.4172/2161-0444.1000189

Copyright: © 2014 Satoh H, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Quercetin, a kind of flavonoids, exerts the cardiovascular actions. In guinea pig ventricular cardiomyocytes, quercetin depresses the action potential duration (APD) and inhibited the underlying ionic currents ICaL.,IKrec. IK1 in cardiomyocytes. In rat aorta, quercetin (0.1 to 100 μM) relaxed the contraction induced by pretreatment with 5 μM norepinephrine (NE) in aconcentration-dependent manner. NG-monomethyl-L-arginine acetate (L-NMMA) at 100 μM reduced the quercetin (100 μM)-induced vasorelaxation from 97.0 ± 3.7% (n=10, p<0.05) to 78.0 ± 11.6% (n=5, p<0.05). Endothelium removal as well attenuated the vasodilatation. In the presence of both 100 μM L-NMMA and 10 μM indomethacin, the quercetin-induced vasorelaxation was further attenuated by high K (30 mM) or 10 μM tetraethylammonium (TEA). Among KCa channel inhibitors, the quercetin-induced vasodilatation was attenuated by 0.3 μM apamin (sensitive to SK), but not by 30 nM charybdotoxin (sensitive to BK and IK). Under KCl-induced vasoconstriction, the quercetin-induced vasorelaxation was attenuated by PK-C inhibitors; Gö6983 (α-, β-, γ-, δ and ζ-sensitive) produced stronger than Ro-31-8425 (α-, β-, γ- and ε-sensitive). In rat mesenteric artery, the quercetininduced vasodilatation was almost resistant to both 100 μM L-NG-nitro arginine methyl ester (L-NAME) and 100 μM indomethacin. The L-NAME/indomethacin-resistant quercetin-induced   was not modified by TEA (1 mM), but was attenuated by endothelium removal and 100 μM 18α- and 50 μM 18β-glychrrhetinic acids (gap junction inhibitors). Therefore, quercetin dilates the vascular smooth muscle mediated by endothelium-dependent and -independent mechanisms.

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