Vasorelaxant effects of 5,7,4'-Trimethoxyflavone from Kaepmferia parviflora in the rat aorta

Abstract

The aim of the present study was to investigate mechanisms underlying vasorelaxation induced by 5,7,4'-trimethoxyflavone (TMF), a major compound isolated from KPE, in the isolated rat aorta. TMF (1-100 μM) caused concentration-dependent vasorelaxations which were reduced by removal of the endothelium and addition of 300 μM NG-nitro L-arginine methyl ester, or 10 μM 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one. However, the effects of TMF were not inhibited by pretreatment with 10 μM indomethacin, 100 μM aminoguanidine, 100 μM 7-nitroindazole. In addition, vasorelaxnt responses to TMF were inhibited by a high concentration of KCl (60 mM), 5 mM tetraethylammonium and 30 μM barium chloride, but not 10 μM glibenclamide and 1 mM 4-aminopyridine. Interestingly, incubation with TMF (10 and 100 μM) for 30 min significantly inhibited contractions to CaCl2 in a Ca2+-free, high K+ buffer. The present findings have shown for the first time that TMF-induced vasorelaxations are partly mediated via endothelium-derived NO, at least in part, through cGMP-dependent pathway. Moreover, activation of K+ efflux and inhibition of extracellular Ca2+ influx are involved in the vasorelaxant effects of TMF. From these findings, TMF acts as a vasodilator and may play an important role in the vasorelaxant effects of KPE. © 2010 Asian Network for Scientific Information.