Possible mechanisms of vasorelaxation for 5,7-dimethoxyflavone from Kaempferia parviflora in the rat aorta

Abstract

The present study investigated the vascular effects of 5,7-dimethoxyflavone (DMF), isolated from the rhizomes of Kaempferia parviflora (KP), on rat isolated aortic rings and its possible mechanisms. DMF (1-100 μm) caused concentration-dependent relaxations in aortic rings precontracted with methoxamine. This effect was significantly reduced by removal of the endothelium, and after pretreatment with NG-nitro-L-arginine methyl ester (L-NAME, 300 μm), indomethacin (10 μm) and 1H-[1,2,4]oxadiazolo-[4, 3-a]quinoxalin-1-one (ODQ, 10 μm), but not 9-(tetrahydro-2-furanyl)-9H- purine-6-amine (SQ22536, 100 μm). Relaxant responses to DMF were significantly inhibited by high KCl (60 mm) in both endothelium-intact and -denuded rings. In addition, the relaxations to DMF were significantly reduced by pretreatment with tetraethylammonium (TEA, 5 mm), glibenclamide (10 μm), 4-aminopyridine (1 mm) or barium chloride (10 μm). Preincubation with DMF (10 and 100 μm) for 30 min significantly inhibited the contractile responses to CaCl2 in a Ca2+-free, high K+ buffer. The present study demonstrated that DMF causes endothelium-dependent relaxation that is partly mediated by NO-cGMP and cyclooxygenase pathways. Interestingly, DMF-induced responses are mainly due to increasing K+ efflux, and inhibition of Ca2+ influx from the extracellular space. The vasodilator effects of DMF provide experimental support for the potential use of KP as a medical plant in the treatment of cardiovascular diseases. © 2010 John Wiley & Sons, Ltd.