The ginsenoside Rg 3 evokes endothelium-independent relaxation in rat aortic rings: role of K + channels

Abstract

The purpose of the present study was to characterize the mechanism underlying the direct relaxing activity of ginsenosides on vascular smooth muscle. The total ginsenoside mixture, ginsenosides from either the protopanaxadiol group or the protopanaxatriol group, and the ginsenoside Rg 3 from the protopanaxatriol group caused a concentration-dependent relaxation of rat aortic rings without endothelium contracted with 25×10 −3 M KCl but affected only minimally those contracted with 60×10 −3 M KCl. Ginsenoside Rg 3 was the most potent relaxing agonist. Relaxations elicited by ginsenoside Rg 3 were markedly reduced by tetraethylammonium, a blocker of non-selective K + channels, but not by glibenclamide, a blocker of ATP-sensitive K + channels. Ginsenoside Rg 3 significantly inhibited Ca 2+-induced concentration–contraction curves and the 45 Ca 2+ influx in aortic rings incubated with 25×10 −3 M KCl whereas these responses were not affected in rings incubated with 60×10 −3 M KCl. Ginsenoside Rg 3 caused a time- and concentration-dependent efflux of 86 Rb from aortic rings that was inhibited by tetraethylammonium but not by glibenclamide. These findings indicate that ginsenoside Rg 3 is a potent inhibitor of vascular smooth muscle tone and that this effect seems to be due to an inhibition of Ca 2+ influx and stimulation of K + efflux, possibly via activation of tetraethylammonium-sensitive K + channels.