The aim of the present study was to examine the effects of platycodin D and D3, which are active components derived from the roots of Platycodon grandiflorum A. DC., on the contractile force of the i3olated rat aorta and blood pressure of the anesthetized rat, and also to elucidate its mechanism of action. Both phenylephrine (an adrenergic α1-receptor agonist) and high potassium (a membrane- depolarizing agent) caused great contractile responses in the isolated aortic strips. Platycodin D at high concentration (24μg/ml) inhibited contractile responses induced by phenylephrine (10-5 M) and high potassium (5.6⁓10⁣2 M), while low concentrations of platycodin D (4∼8μg/ml) did not affect those responses. However, platycodin D3 (8∼32μg/ml) did not alter the contractile responses evoked by phenylephrine and high K⁢. Interestingly, the infusion of platycodin D3 (1.0 mg/kg/30 min) significantly reduced the pressor responses induced by intravenous norepinephrine. However, platycodin D3 (1.0 mg/kg/30 min) did not affect them. Taken together, these results show that intravenously administered platycodin D depresses norepinephrine-induced pressor responses in the anesthetized rat, at least partly through the blockade of adrenergic α1-receptors. Platycodin D also caused vascular relaxation in the isolated aortic strips of the rat via the blockade of adrenergic α1-receptors, in addition to an unknown direct mechanism. However, platycodin D3 did not affect both norepinephrine-induced pressor responses and the isolated rat aortic contractile responses evoked by phenylephrine and high potassium. Based on these results, there seems to be much difference in the mode of action between platycodin D and platycodin D3.