Vascular Pharmacology of Mokuboito (Mu-Fang-Yi-Tang) and Its Constituents on the Smooth Muscle and the Endothelium in Rat Aorta

Pharmacological actions of Mokuboito and its constituents (Sinomenium acutum and sinomenine) on rat aorta were examined. Mokuboito and S. acutum at 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 and S. acutum dilated 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 and S. acutum was attenuated by indomethacin, L-NMMA and nicardipine. Propranolol decreased the vasorelaxation induced by Mokuboito, but not by S. 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 (PGI2 and NO from endothelium) and by endothelium-independent mechanisms (Ca2+ influx control on smooth muscle cells). Simultaneously, Mokuboito and S. acutum cause the vasoconstrictions mediated through α-adrenoceptor stimulation, but not sinomenine. Also, Mokuboito and sinomenine possess β-adrenoreceptor stimulating action, but not S. acutum.