Pharmacological actions of Mokuboito and its constituents (Sinomenium acutumand sinomenine) on rat aorta were examined. Mokuboito andS. acutumat lower concentrations (0.03–1 mg ml−1) contracted the non-loaded aorta, but at higher concentrations (1–3 mg ml−1), reversed to dilate it. The vasoconstriction was blocked by phentolamine (10 μM). Sinomenine failed to exhibit the vasoconstriction. On the other hand, Mokuboito andS. acutumdilated the NE (5 μM)-induced vasoconstriction: at 3 mg ml−1, by 98.9 ± 2.5% (n= 6,P< 0.01) and 97.0 ± 4.8% (n= 6,P< 0.01). Vasorelaxation induced by Mokuboito andS. acutumwas attenuated by indomethacin, L-NMMA and nicardipine. Propranolol decreased the vasorelaxation induced by Mokuboito, but not byS. acutum. Sinomenine also relaxed the constriction and at 100 μM, by 68.8 ± 5.1% (n= 7,P< 0.01). This vasorelaxation was attenuated by indomethacin, L-NMMA and nicardipine, and also by propranolol. Therefore, these results indicate that Mokuboito and its constituents exert both vasodilating actions mediated by endothelium-dependent mechanisms (PGI2and NO from endothelium) and by endothelium-independent mechanisms (Ca2+influx control on smooth muscle cells). Simultaneously, Mokuboito andS. acutumcause the vasoconstrictions mediated through α-adrenoceptor stimulation, but not sinomenine. Also, Mokuboito and sinomenine possess β-adrenoreceptor stimulating action, but notS. acutum.