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 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.