Ginsenoside Rg3 mediates endothelium-dependent relaxation in response to ginsenosides in rat aorta:: role of K+ channels

The aim of the present study was to characterize the endothelium-dependent relaxation elicited by ginsenosides, a mixture of saponin extracted from Panax ginseng, in isolated rat aorta. Relaxations elicited by ginsenosides were mimicked by ginsenoside Rg(3) and ginsenoside Rg(1), two major ginsenosides of the protopanaxatriol group. Ginsenoside Rg(3) was about 100-fold more potent than ginsenoside Rg(1). The endothelium-dependent relaxation in response to ginsenoside Rg(3) was associated with the formation of cycle GMP. These effects were abolished by N-G-nitro-L-arginine and methylene blue. Relaxations in response to ginsenoside Rg(3) were unaffected by atropine, diphenhydramine, [D.Pro(2), D-Trp(7.9)]substance P, propranolol, nifedipine, verapamil and glibenclamide but were markedly reduced by tetraethylammonium. Tetraethylammonium modestly reduced the relaxation induced by sodium nitroprusside. These findings indicate that ginsenoside Rg(3) is a major mediator of the endothelium-dependent nitric oxide-mediated relaxation in response to ginsenosides in isolated rat aorta, possibly via activation of tetraethylammonium-sensitive K+ channels. (C) 1999 Elsevier Science B.V. All rights reserved.