In the present study, the effects of the bioflavonoid chrysin (5,7-dihydroxyflavone) were analyzed on the perfusion pressure of isolated mesenteric vascular bed. The vasorelaxant effects of chrysin were more potent on intact endothelium than on denuded vessels. This endothelium-dependent response induced by chrysin was inhibited in the presence of N(G)-nitro-L-arginine methyl ester (L-NAME), KCl, tetraethylammonium (TEA), BaCl(2), TEA plus L-NAME, and ouabain plus BaCl(2), while incubations with indomethacin and glibenclamide did not modify the response induced by this bioflavonoid. Neither gap junction inhibition with carbenoxolone nor epoxyeicosatrieconic acid synthesis inhibition with sulfaphenazole (selective CYP 2C/3A inhibitor) or 7-ethoxyresorufin (selective CYP 1A inhibitor) inhibited the chrysin-induced relaxation. Moreover, chrysin increased L-NAME-sensitive cGMP accumulation in intact vascular mesenteric preparation. In conclusion, chrysin shows vasodilator effects on resistance vessels, which depend partially on the functional endothelium and appear to be related to the NO/cGMP pathway and, possibly to the release of endothelium-derived hyperpolarizing factor.
Copyright 2004 S. Karger AG, Basel.