Department of Pharmacology, Division of Traditional Herbal Medicine, Nara Medical University, Nara 634-8521, Japan.
Korean J Physiol Pharmacol. 2009 Oct;13(5):361-5. doi: 10.4196/kjpp.2009.13.5.361. Epub 2009 Oct 31.
Effects of quercetin, a kind of flavonoids, on the vasodilating actions were investigated. Among the mechanisms for quercetin-induced vasodilatation in rat aorta, the involvement with the Ca(2+) activated K(+) (K(Ca)) channel was examined. Pretreatment with NE (5 microM) or KCl (60 mM) was carried out and then, the modulation by quercetin of the constriction was examined using rat aorta ring strips (3 mm) at 36.5. Quercetin (0.1 to 100 microM) relaxed the NE-induced vasoconstrictions in a concentration-dependent manner. NO synthesis (NOS) inhibitor, NG-monomethyl-L-arginine acetate (L-NMMA), at 100 microM reduced the quercetin (100 microM)-induced vasodilatation from 97.8+/-3.7% (n=10) to 78.0+/-11.6% (n=5, p<0.05). Another NOS inhibitor, L-NG-nitro arginine methyl ester (L-NAME), at 100 microM also had the similar effect. In the presence of both 100 microM L-NMMA and 10 microM indomethacin, the quercetin-induced vasodilatation was further attenuated by 100 microM tetraethylammonium (TEA, a K(Ca) channel inhibitor). Also TEA decreased the quercetin-induced vasodilatation in endothelium-denuded rat aorta. Used other K(Ca) channel inhibitors, the quercetin-induced vasodilatation was attenuated by 0.3 microM apamin (a SK channel inhibitor), but not by 30 nM charybdotoxin (a BK and IK channel inhibitor). Quercetin caused a concentration-dependent vasodilatation, due to the endothelium-dependent and -independent actions. Also quercetin contributes to the vasodilatation selectively with SK channel on smooth muscle.
研究了一种黄酮类化合物槲皮素对血管舒张作用的影响。在研究槲皮素诱导的大鼠主动脉舒张的机制中，研究了与 Ca2+激活的 K+（KCa）通道有关的机制。使用 NE（5 μM）或 KCl（60 mM）进行预处理，然后在 36.5 下使用大鼠主动脉环条（3 mm）检查槲皮素对收缩的调制。槲皮素（0.1 至 100 μM）以浓度依赖性方式松弛 NE 诱导的血管收缩。100 μM 的一氧化氮合酶（NOS）抑制剂，NG-单甲基-L-精氨酸乙酸盐（L-NMMA）将槲皮素（100 μM）诱导的血管舒张从 97.8+/-3.7%（n=10）降低至 78.0+/-11.6%（n=5，p<0.05）。另一种 NOS 抑制剂，L-NG-硝基精氨酸甲酯（L-NAME）在 100 μM 时也具有相似的作用。在存在 100 μM L-NMMA 和 10 μM 吲哚美辛的情况下，100 μM 四乙铵（TEA，一种 KCa 通道抑制剂）进一步减弱了槲皮素诱导的血管舒张。TEA 还降低了去内皮大鼠主动脉中槲皮素诱导的血管舒张。使用其他 KCa 通道抑制剂，0.3 μM 蜂毒肽（SK 通道抑制剂）减弱了槲皮素诱导的血管舒张，但 30 nM 霍乱毒素（BK 和 IK 通道抑制剂）则没有。槲皮素引起浓度依赖性血管舒张，这是由于内皮依赖性和非依赖性作用。槲皮素还通过平滑肌上的 SK 通道选择性地有助于血管舒张。
