卡托普利及SNP对VSMC中ET-1释放的作用.docVIP

卡托普利及SNP对VSMC中ET-1释放的作用 卡托普利及SNP对VSMC中ET-1释放的作用 2010-01-14 丛洪良　黄体钢　周丽娟　宋昱　马向虹　王伟　刘洪梅 　　【摘要】　目的　探讨卡托普利及SNP对培养的大鼠VSMC释放ET-1的影响及相互关系。方法　在大鼠VSMC培养液中置入不同浓度卡托普利及/或SNP后，用放免法测定ET-1。结果　卡托普利及SNP均可减低因AngⅡ引起VSMC分泌增加的内皮素量，AngⅡ水平与VSMC分泌ET-1量呈正相关。结论　ET-1通过抑制VSMC内源性NO的产生加速AS的发生及发展，ACEI或NO抑制ET-1释放，可减缓AS形成。 　　【关键词】　卡托普利　硝普钠　内皮素　一氧化氮　血管平滑肌细胞 The releasing effected of captopril and sodium nitroprusside on endothelin-1 in vascular smooth muscle cell 　Cong Hongliang, Huang Tigang, Zhou Lijuan, et al. Tianjin Cardiovascular Institute, Tianjin 300211 　　【Abstract】　Objective　Investigating the influence of captopril and SNP on releasing ET-1 in cultured VSMC of rat. Methods　Measuring the endothelin-1 level through radioimmunology assay in various concentration of captopril and/or sodium nitroprusside in cultured vascular smooth muscle cell of rat. Results　The results show that both captopril and SNP could reducing the high ET-1 level of VSMC which were caused by AngⅡ. There were a linear relationship between AngⅡ level and ET-1 production (r=0.760 1,P＜0.001).Conclusion　Endothelin-1 maybe accelerating the atherosclerosis formation and developing through inhibiting endogenous NO produced by VSMC. ACEI or NO, inhibiting ET-1 release, may reduce atherosclerosis formation. 　　【Key words】　Captopril Sodium nitroprusside Endothelin-1 Nitric oxide Vascular smooth muscle cell 　　血管紧张素转换酶抑制剂(ACEI)已被公认为高血压、冠心病有效药物之一，并已广泛应用。硝普钠(Sodium Nitroprusside, SNP)为血管扩张剂，由于在体内产生NO，被认为是一种NO供体。NO抑制血小板聚集、血管平滑肌细胞(VSMC)增生及白细胞对内皮细胞(EC)粘附，对限制动脉粥样硬化(AS)的局部血管损伤起重要作用［1］。但ACEI及一氧化氮(NO)对局部损伤所起的保护作用是否与VSMC释放的内皮素(ET-1)减少有关，尚少见报道。本研究的目的是探讨卡托普利及SNP对培养大鼠VSMC释放ET-1的影响及相互关系。 材料与方法 　　1.大鼠VSMC培养、鉴定与分组 　　大鼠VSMC培养为组织贴块法［2］。应用透射电镜鉴定VSMC，待VSMC长满呈亚融合状，消化成细胞悬液铺24孔板，每孔为3.1×104细胞数，于CO2孵育箱静置48小时，弃上清液，设定每六孔为一组。实验组分别予以含AngⅡ80 pg/mL、160 pg/mL、320 pg/mL、640 pg/mL,AngⅡ640 pg/mL+卡托普利100μg/mL,AngⅡ640 pg/mL+卡托普利100 μg/mL+SNP 10-5mol/mL及加入含SNP 10-5mol/mL的M199培养液；对照组加入正常M199培养液。CO2孵育箱孵育36小时后取细胞培养液进行鉴定。 　　2.主要试剂及测试盒 　　AngⅡ粉剂(购自北京同正生物技术公司)，ET-1放免