Investigation of the flower buds and peduncles of Lindera megaphylla led to the isolation of six aporphine alkaloids, dicentrine, N-methylnanigerine, dicentrinone, dehydrodicentrine, O-methylbulbocapnine, and cassameridine. Three flavonoid glycosides, isoquercitrin, tiliroside, and rutin, were also isolated. O-Methylbulbocapnine inhibited platelet aggregation and also suppressed the contraction of the rat thoracic aorta, but to a much lesser extent than did dicentrine. In the course of our studies on the development of naturally occurring antiplatelet agents, we have reported that dicentrine [1] from the roots of Lindera megaphylla possessed antiplatelet aggregation, vasorelaxant, and antiarrhythmic activities (1-3). In our continuing research on this plant, six aporphine alkaloids, namely, dicentrine [1], N-methylnanigerine, O-methylbulbocapnine [2] (4), dehydrodicentrine [3] (6), dicentrinone [4] (4,5), and cassameridine (7), along with three flavonoid glycosides, isoquercitrin, tiliroside, and rutin, were isolated from the flower buds and peduncles of L. megaphylla. The identifications of alkaloids 2-4 and cassameridine were carried out by comparison of their data with published reports (4-7), and the other known compounds were identified by comparison (eims, nmr, ir, tlc) with authentic samples from this laboratory. Copies of the original spectra of these known compounds may be obtained from the senior author. The effects on platelet aggregation were tested using washed rabbit platelets. As shown in Table 1, compounds 3 and 4, at 300 μM, caused spontaneous aggregation of platelets in the absence of any inducers. Compound 2, at 300 μM, exhibited 20 to 30% inhibitory activities on arachidonic acid- and collagen-induced platelet aggregation, but 1 showed complete inhibition at the same concentration. The inhibitory effects of the isolated compounds on the contractions of the rat aorta induced by norepinephrine and high potassium are shown in Table 2. Compounds 3 and 4, at 120 μM, had no inhibitory effect. Compound 2 exhibited inhibitory effects, at 60 and 120 μM, on norepinephrine- and high K+-induced contractions of the rat aorta, while 1 showed a similar inhibition at 9 μM to that of 120 μM of compound 2. This means 1 is over ten times more potent than 2. Thus, compound 2 is an inhibitor of both platelet aggregation and vasoconstriction. The vasorelaxation is not due to the increase of prostaglandin I2 production inasmuch as it inhibits arachidonic acid-induced platelet aggregation. Furthermore, when the endothelium of the aorta was denuded the inhibitory effect of compound 2 on vasoconstriction was unaffected. Further experiments are needed to elucidate the mechanisms of action.