摘要
目的观察杭白菊总黄酮(TFCM)的舒血管作用并探讨其作用机制。方法大鼠胸主动脉环张力测定法。结果在内皮完整及去内皮血管上,TFCM均浓度依赖性地降低苯肾上腺素(PE)预收缩血管的张力,拮抗高钾引起的血管收缩;TFCM使PE收缩曲线非平行右移,且使最大张力减小;L-NAME、亚甲蓝和吲哚美辛能显著减弱TFCM的血管舒张作用;TFCM可以显著对抗无钙环境下以及无钙环境下渐加钙由PE引起的血管收缩。结论TFCM对血管的舒张作用表现为内皮依赖性,其舒张作用与其直接抑制电压依从性钙通道、受体操纵性钙通道、细胞内钙释放有关。
Objective： To investigate the vasodilative effect of TFCM and its underlying mechanism. Methods： The effects of TFCM on the contraction of rat thoracic aorta rings in organ bath were measured. Results： TFCM could cause concentration-dependent relaxation of endothelium-intact or endothelium-denuded aorta rings precontracted with phenylephrine （PE , 10^-6 mol/L） and resist vasoconstriction induced by high level of K^＋ （6 × 10^-2 mol/L ）. TFCM caused unparallel shift of the PE concentration-response curve to the right and reduced the maximal contraction induced by PE. L-NAME , methylene blue and indomethacin could reduce the vasodilative effect of TFCM significantly. TFCM could obviously reduce transient vasoconstriction in free Ca^2＋ solution and resist steady vasoconstriction induced by PE in free Ca^2＋ solution when concentration of Ca^2＋ increased. Conclusion： TFCM induced endothelium-dependent relaxation in rat thoracic aorta. The mechanism is related to inhibition of voltage-dependent Ca^2＋ channel（VDC） , receptor-operate Ca^2＋ channel （ROC） , release of intracellular Ca^2＋.
出处
《杭州师范学院学报（自然科学版）》
CAS
2005年第6期411-414,共4页
Journal of Hangzhou Teachers College(Natural Science)
关键词
杭白菊总黄酮
血管平滑肌
收缩
钙通道
total flavones from Crysanthemum morifolium Ramat. cv. Hangju （TFCM）
vascular smooth muscle
vasoconstriction
calcium channel
