摘要
采用fura 2荧光测定细胞 [Ca2 +]i 变化技术 ,在培养的牛主动脉内皮细胞上观察ATP和凝血酶诱导的Ca2 +内流的特性 .ATP和凝血酶均能诱导内皮细胞 [Ca2 +]i 呈双相升高 ,它们诱导的Ca2 +释放是环匹阿尼酸 (CPA)敏感Ca2 +池的一部分 .ATP诱导的Ca2 +释放和Ca2 +内流不完全通过激活磷脂酶C介导 ,而凝血酶诱导的Ca2 +释放和Ca2 +内流则完全通过激活磷脂酶C介导 .硝苯地平对ATP和凝血酶诱导的Ca2 +内流均无影响 ;SK&F 96 36 5与三七皂甙 2A对凝血酶诱导的Ca2 +内流没有影响 ,但可抑制ATP诱导的Ca2 +内流 ,且此作用比它们对CPA诱导Ca2 +内流的抑制作用小 .SK&F 96 36 5和三七皂甙 2A敏感的Ca2 +内流的特性不同 .结果表明ATP和凝血酶激活不同受体 ,引起Ca2
The effects of drugs on intracellular calcium concentration([Ca 2+ ] i) were investigated with fura-2 fluorescence technique to investigate ATP and thrombin-induced Ca 2+ entry in bovine aortic endothelial cells(BAEC). It was found that application of ATP and thrombin gave rise to biphasic [Ca 2+ ] i elevation. ATP or thrombin only triggered a fraction of cyclopiazonic acid(CPA)-sensitive Ca 2+ store, which was enough to activate Ca 2+ entry. The Ca 2+ release induced by thrombin resulted from the activation of phospholipase C(PLC), whereas the PLC-independent mechanism was involved in ATP-induced Ca 2+ release. Nifedipine had no effect on ATP and thrombin- induced Ca 2+ entry. SK&F 96365 and ginsenoside-2A inhibited both ATP and CPA-induced Ca 2+ entry, however no effect of them on thrombin-induced Ca 2+ entry was found. The inhibitory effects of SK&F 96365 and ginsenoside-2A on CPA-induced Ca 2+ entry were less than that on ATP-induced Ca 2+ entry. The Ca 2+ influx sensitive to SK&F 96365 was not the same as that to ginsenoside-2A. These observations suggest that both ATP and thrombin evoke Ca 2+ release and Ca 2+ influx by activation of different receptor. However their mechanisms appear different.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
2001年第2期131-136,共6页
Chinese Journal of Pharmacology and Toxicology
基金
国家科技部攀登计划! (国科基字 [1999]0 45号 )
国家自然科学基金资助项目! ( 39770 85 8)
广东省中医药管理局科研基金资助项
关键词
钙通道
腺苷三磷酸
凝血酶
血管内皮细胞
药理学
endothelium, vascular
cells,cultured
calcium channels
adenosine triphosphate
thrombin
