Vascular relaxation induced by aqueous extract of Lespedeza cuneata via the NO-cGMP pathway.

The aqueous extract of Lespedeza cuneata G. Don. (ALC) induced vasorelaxation of phenylephrine precontracted aorta in a dose-dependent manner. This effect disappeared in the absence of functional endothelium. Pretreatment of the aortic tissues with N(G)-nitro-L-arginine methyl ester (L-NAME), or 1H-[1,2,4]-oxadiazole-[4,3-α]-quinoxalin-1-one (ODQ) blocked ALC-induced vascular relaxation. Incubation of endothelium-intact thoracic aortic rings with ALC increased cGMP production. ALC-induced cGMP production was blocked by pretreatment with L-NAME or ODQ. ALC-induced vascular relaxation was also markedly attenuated by addition of verapamil or diltiazem, but was not blocked by pretreatment with indomethacine, glibenclamide, tetraethylammonium, atropine, or propranolol. The results suggest that ALC dilates vascular smooth muscle via endothelium-dependent NO-cGMP signaling.