Vascular relaxation by the methanol extract of Sorbus cortex via NO-cGMP pathway.

The methanol extract of Sorbus commixta cortex (MSC) induced relaxation of the phenylephrine-precontracted aorta in a dose-dependent manner, which was disappeared by removal of functional endothelium. Pretreatment of the aortic tissues with N(G)-nitro-L-arginine methyl ester (L-NAME), methylene blue, or 1H-[1,2,4]-oxadiazole-[4,3-alpha]-quinoxalin-1-one (ODQ) inhibited the vascular relaxation induced by MSC. MSC-induced vascular relaxations were also markedly attenuated by addition of verapamil or diltiazem, while the relaxant effect of MSC was not blocked by pretreatment with indomethacine, glibenclamide, tetraethylammonium (TEA), atropine, or propranolol, respectively. Incubation of endothelium-intact carotid arteries or of human umbilical vein endothelial cells (HUVECs) with MSC increased the production of guanosine 3',5'-cyclic monophosphate (cGMP). Moreover, MSC-induced cGMP production was effect was blocked by pretreatment with L-NAME or ODQ. These results suggest that MSC dilates vascular smooth muscle via endothelium-dependent nitric oxide-cGMP signaling pathway, possible involvement of L-type Ca(2+) channel.