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为了探讨内皮细胞损伤和糖皮质激素对血管平滑肌细胞（ＶＳＭＣ）血管紧张素Ⅱ（ＡｎｇⅡ）１型受体（ＡＴ１）基因ｍＲＮＡ表达和细胞超微结构的影响。本试验将３５只家兔随机分为５组，每组７只。１．对照组２．内膜损伤组：用球囊进行髂动脉内膜损伤。３．内膜损伤＋ＲＵ４８６组：髂动脉内膜损伤后，给家兔口服糖皮质激素受体拮抗剂（ＲＵ４８６）。４．地塞米松组：腹腔注射地塞米松（７ｍｇ／ｋｇ／ｄ）。５．地塞米松＋ＲＵ４８６组：地塞米松和ＲＵ４８６同时给药。各实验组家兔４周后处死，用ＲＴ－ＰＣＲ的方法检测髂动脉ＶＳＭＣＡＴ１的基因表达。透射电镜观察ＶＳＭＣ的超微结构。结果表明内皮细胞损伤和地塞米松可使ＶＳＭＣ的ＡＴ１ｍＲＮＡ的表达上调（Ｐ＜０．０１），糖皮质激素受体阻断剂米非司酮（ＲＵ４８６）可阻断这种表达的上调。内皮细胞损伤和地塞米松还能使ＶＳＭＣ内粗面内质网增多，肌丝减少，促进ＶＳＭＣ向合成型转化。所以，内皮细胞损伤和地塞米松等应激因素可通过激活糖皮质激素受体，诱导ＡＴ１的基因表达，促进ＶＳＭＣ增殖，这个过程与动脉粥样硬化的发生有关。
To investigate the effects of endothelial cell injury and glucocorticoids on mRNA and cell ultrastructure of angiotensin Ⅱ type 1 receptor (AT1) in vascular smooth muscle cells (VSMCs). This experiment will be 35 rabbits were randomly divided into 5 groups of 7. 1. Control group 2. Intimal injury group: Balloon Iliac artery intimal injury. 3. Intimal Injury + RU486 Group: Rabbit was given glucocorticoid receptor antagonist (RU486) after injury of the iliac artery. 4. Dexamethasone group: Dexamethasone (7 mg / kg / d) was injected intraperitoneally. 5. Dexamethasone + RU486 group: Dexamethasone and RU486 administered simultaneously. The rabbits in each experimental group were sacrificed after 4 weeks, and the gene expression of VSMCAT1 in iliac artery was detected by RT-PCR. The ultrastructure of VSMC was observed by transmission electron microscope. The results showed that endothelial cell injury and dexamethasone up-regulated VSMC AT1mRNA expression (P <0.01), and glucocorticoid receptor blocker mifepristone (RU486) blocked the up-regulation of this expression. Endothelial cell damage and dexamethasone can also increase the number of rough endoplasmic reticulum in VSMC, reduce myofilament, VSMC synthesis to promote conversion. Therefore, endothelial cell injury and dexamethasone and other stress factors can activate glucocorticoid receptor, induced AT1 gene expression and promote VSMC proliferation, the process of atherosclerosis with the occurrence.