摘要
研究黄芩苷对大鼠离体胸主动脉环的舒张作用并探讨其可能的机制。记录去甲肾上腺素(NE)和KCl预收缩的大鼠离体主动脉环张力变化,观察黄芩苷的舒血管作用及不同工具药对其影响。实验发现黄芩苷对NE和KCl引起的去内皮和内皮完整大鼠胸主动脉环的收缩均有舒张作用;L-硝基精氨酸甲酯、亚甲蓝不能抑制黄芩苷对大鼠胸主动脉环的舒张作用,吲哚美辛能显著抑制;钾离子通道阻断剂4-氨基吡啶、四乙基胺、BaCl2不能抑制黄芩苷对胸主动脉环的舒张作用,格列苯脲能抑制黄芩苷的舒张作用;无钙环境下,黄芩苷预处理对NE收缩有明显抑制作用。因此,黄芩苷具有浓度依赖性血管舒张作用,此作用具有内皮依赖性和非内皮依赖性特点,内皮依赖性收缩可能与前列环素途径有关,非内皮依赖机制可能与KATP通道及钙离子通道有关。
To investigate the vasodilation effect of baiealin and its possible mechanism,isotonic tension of thoracic aortic rings precon- tracted with norepineprine and KC1 was recorded. The vasodilation of baicalin and the influence of various drugs were observed in the rings with endothelium intact or endothelium denuded. Baicalin caused concentration-dependent relaxation in thoracic aortas with or without endothelium. NG-nitro-L-argininemethylester and methylene blue had no effect on the vasodilation of baicalin while thoracic aortas were precontracted by NE, but indomethacin blocked the vascular effect of baicalin. Glibenclamide attenuated the vasodilation effect of baicalin, but 4-aminopyridine, tetraethylamonium and BaC12 had no significant effect on it. In the absence of extracellular Ca2＋ ,pre-incubation of the aortic rings with baicalin reduced significantly the contraction induced by NE. Baicalin induced a dose- dependent, endothelium-dependent and endothelium-independent relaxation on rat isolated aorta rings. Moreover, PGI2 pathway might be involved in the endothelium-dependent relaxation. The mechanism might be related to the inhibition of KATP channel and Ca2＋ channel.
出处
《药物生物技术》
CAS
2013年第2期146-148,共3页
Pharmaceutical Biotechnology
基金
国家自然科学基金(No.81073010)
