There have been conflicting reports on vascular response to Panax ginseng. The conflicting reports may be due to difference of ingredient of Panax ginseng. The aim of the present study was to investigate the effect of saponin, the main ingredient of Panax ginseng, on the vascular contractility.

The rabbit aortic rings were cut and mounted on the force transducer to record an isometric tension on polygraph. To elucidate the mechanism of saponin effect on vascular smooth muscle, the contractility of the vascular smooth muscle were measured under varying experimental condition.

1) When the aortic rings were precontracted with norepinephrine, saponin caused biphasic(initial relaxation-sustained contraction) dose-response in the endothelium dependent manner. But saponin had no effect on the resting tension.

2) When EDRF inhibitors such as methylene blue(10^-5M), hemoglobin(10^-5M), N-ω-nitro-L-arginine(100µM) were added to precontracted ring with norepinephrine, the initial relaxation caused by 2mg% saponin was inhibited.

3) When Ca²⁺-channel blocker, nifedipine(5×10^-7M), was added to precontracted rings with norepinephrine, the sustsined contraction by saponin was inhibited. 4) When hemoglobin(10^-5M) was added to precontracted rings with norepinephrine, the contractility by norepinephrine was increased and this effect was further augmented by 2mg% saponin.

From the above results, it may be concluded that saponin stimulated the release of both an endothelium-dependent relaxing factor and endothelium-dependent contracting factor.