Role of gap junction involved with endothelium-derived hyperpolarizing factor for the quercetin-induced vasodilatation in rat mesenteric artery.

Modulation of vasodilating actions by quercetin, a kind of flavonoid, was investigated using rat mesenteric arterial ring strips. Ring strips (1mm) of rat mesenteric artery were used. The specimens were kept at 36.5 °C in Krebs-Henseleit solution oxygenated with 95% O(2) and 5% CO(2). Quercetin (0.1 to 100 μM) dilated the contraction induced by norepinephrine (1 μM) in a concentration-dependent manner. The quercetin-induced vasodilatation was almost resistant to both 100 μM L-N(G)-nitro arginine methyl ester (L-NAME) and 100 μM indomethacin. At 1mM tetraethylammonium (a KCa channel inhibitor) decreased the quercetin-induced vasodilatation, which was resistant to L-NAME and indomethacin, but not significantly. L-NAME- and indomethacin-resistant quercetin-induced vasodilatation was significantly attenuated by 100 μM 18α- and 50 μM 18β-glycyrrhetinic acids (gap junction inhibitors). Endothelium removal as well significantly attenuated the vasodilatation to the same extent. These results indicate that quercetin dilates the mesenteric artery via endothelium-dependent mechanisms, and the dilatation is mainly mediated by gap junctions closely involved with endothelium-derived hyperpolarizing factor (EDHF).