Ginsenoside Rg 3 mediates endothelium-dependent relaxation in response to ginsenosides in rat aorta: role of K + channels

Abstract

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 cyclc 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.