It has been known that Ginseng extract causes the hypotensive action while it rather produces the hypertensive action. Some studies have suggested that Ginseng extract causes a biphasic response on blood pressure, namely, transient fall followed by prolonged elevation. It has been also shown that administration of Korean Red Ginseng powder has no effect on blood pressure in normotensive and hypertensive rats. The present study was designed to examine the effect of total Ginseng saponin on contractile responses of vasoconstrictors in the rat aorta and to establish the mechanism of its action.

The ring segment of aorta was mounted in a muscle bath filled with oxygenated Krebs solution for the measurement of isometric tension. After the equilibration period, under the presence of total Ginseng saponin, isometric tension induced by some vasoconstrictors were observed and compared to the control responses. The data were expressed as % of the control tension.

Phenylephrine (an adrenergic α₁-receptor agonist) and high potassium (a membrane depolarizing agent) caused greatly contractile responses in the rat aorta, respectively. However, in the presence of total ginseng saponin (600 g/ml), the contractile responses of phenylephrine (10^-6 and 10^-5 M) and high potassium (3.5 × 10^-2 and 5.6 × 10^-2 M) were markedly potentiated whereas prostglandin F₂α(5 × 10^-6 M)-induced contractile responses was not affected. The contractile responses induced by phenylephrine (10^-5 M) and high potassium (3.5 × 10^-2 M) even under the presence of total ginseng saponin (600 g/ml) were greatly inhibited by the pretreatment of nicardipine (10^-6 M), a calcium channel blocker.

Taken together, these experimental results suggest that total ginseng saponin can enhance the contractile responses evoked by stimulation of adrenergic α₁-receptor and the membrane depolarization in the isolated rat aortic strips, which seems to be associated to calcium influx.