摘要
目的观察大黄素的舒血管作用并探讨其舒张作用机制。方法采用大鼠胸主动脉环张力测定法。结果大黄素对苯肾上腺素(PE,10-6mol.L-1)预收缩的内皮完整或去内皮血管环均产生浓度依赖性的舒张作用;对高钾预收缩血管环也产生浓度依赖性的舒张作用。普奈洛尔(propranolol,1.0×10-6mol.L-1)对大黄素的舒血管作用无显著影响;非特异性钾通道抑制剂CsCl和Ca2+激活钾通道抑制剂四乙胺(TEA,5.0×10-3mol.L-1)预处理能显著减弱大黄素的舒血管作用;大黄素可以显著地对抗无钙环境下由咖啡因或无钾环境下由PE引起的血管收缩。结论大黄素非内皮依赖性血管舒张作用与其直接抑制细胞外钙内流、肌浆网内钙离子的释放,以及激活Ca2+激活钾通道(Kca)有关,而与β-受体无关。
OBJECTIVE To investigate the vasodilating effects and underlying mechanism of emodin. METHODS The tension of rat thoracic aorta tings was measured. RESULTS Emodin caused concentration-dependent relaxation in KCl and PE pre-treated aorta rings with or without endothelium. Propranolol did not affect the effect of emodin on rat thoracic aorta rings. The relaxation response of emodin was significantly inhibited by petassittm channel inhibitors CsCl and TEA, respectively. Emodin also inhibited the transient contraction by caffeine in free Ca^2＋ solution, or by PE in K^＋-free solution, respectively. CONCLUSION Emodin induces endothelittm-independent relaxation in rat thoracic aorta, The inhibition of Ca^2＋ entry, the release of intracellular Ca^2＋ , and the activation of Ca^2＋ -activated K^ channel may contribute to its vasorelaxation effect. On the other band,β-drenoceptor is not involved in this process.
出处
《中国药学杂志》
CAS
CSCD
北大核心
2006年第7期505-508,共4页
Chinese Pharmaceutical Journal
基金
国家自然科学基金资助项目(30471956)
浙江大学医学院2005年科研启动基金
