Possible Involvement of Ca2+ Activated K+ Channels, SK Channel, in the Quercetin-Induced Vasodilatation

Abstract

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.