Mechanisms for the vasodilations induced by Ginkgo biloba extract and its main constituent, bilobalide, in rat aorta

Abstract

Vasodilating actions of Ginkgo biloba extract (GBE) and bilobalide, a main constituent, were examined using rat aorta ring strips. GBE at the concentration ranges from 0.03 to 3 mg/ml had a potent concentration-dependent relaxation, reaching 70 ± 4.5% (n = 6, P < 0.001) at 3 mg/ml. Bilobalide at 0.1 to 100 μM also caused the relaxation in a concentration-dependent manner. At 100 μM, bilobalide caused dilation by 17.6 ± 3.9% (n = 7, P < 0.05). NG-monomethyl-L-arginine acetate (L-NMMA)(100 μM), an NO synthesis inhibitor, reduced the vasodilation of GBE (3 mg/ml) to 57.6 ± 2.5% (n = 6, P < 0.05), and was accompanied with a decrease in the rate of relaxation. Tetraethylammonium (TEA)(100 μM), a Ca 2+-activated K + channel inhibitor, also decreased the GBE (3 mg/ml)-induced relaxation to 63.1 ± 4.6% (n = 6), but not significantly. Indomethacin tended to reduce the GBE (3 mg/ml)-induced vasorelaxation to 67.3 ± 4.1% (n = 6). In contrast, the vasorelaxation of GBE (3 mg/ml) was strongly attenuated to 53 ± 6.1% (n = 7, P < 0.05) in Ca 2+-free medium. Similarly, the vasorelaxation induced by bilobalide significantly decreased both by pretreatment with NO inhibitor (L-NMMA) and in Ca 2+-free solution. These results indicate that the relaxation induced by GBE would be due to the inhibition of Ca 2+ influx through the Ca 2+ channel and the activation of NO release, and might be in part due to the inhibitions of Ca 2+-activated K + current and PGI 2 release, in the endothelium and aortic vascular muscles. Bilobalide possesses the similar mechanisms for the vasodilation.