摘要
目的:观察阿托伐他汀对自发性高血压大鼠(SHR)血压的影响,初步探讨其调节血压的机制。方法:SHR(n=12)随机分为SHR对照组、阿托伐他汀治疗组,同龄WKY大鼠(n=6)作为正常血压对照组,灌胃给药6周。采用尾袖法测量大鼠尾动脉收缩压,硝酸还原酶法测定血清NO浓度,化学比色法检测NOS活性和ROS活性,放免分析法测定心肌AngⅡ含量,透射电镜观察主动脉内皮超微结构改变。结果:阿托伐他汀治疗6周后,SHR治疗组SBP明显下降(P<0.01);心肌AngⅡ浓度明显下降(P<0.05);血清NO浓度和主动脉NOS活性明显增高(P<0.01,P<0.05),血清ROS水平明显降低(P<0.05)并明显改善SHR主动脉内皮的超微结构改变。结论:阿托伐他汀可降低SHR血压,可能是通过增加主动脉NOS活性,升高血清NO含量,减少ROS生成,改善血管内皮功能而发挥降低血压作用。
Objective:To investigate the effects of atorvastatin on blood pressure in spontaneously hypertensive rats (SHR) for exploring the potential mechanisms. Methods: SHR ( n = 12) were randomly divided into SHR control and atorvastatin group, Wistar-Kyoto rats of agematched were selected as normal control group with measurement of the systolic blood pressure by tail-cuff method. Nitric oxide (NO) and reactive oxygen species (ROS) levels in serum, Ang Ⅱ levels in myocardium and nitric oxide synthase (NOS) activity in aortic were measured by ni- trate reductase method, chemistry colorimetry, raddioimmunossay respectively. Transmission electron microscope was used to observe the aortic ultrastructure. Results : After 6 weeks treatment,as compared atorvastatin grou with SHR control group, SBP, the AngⅡ levels in myocardium and serum and ROS levels was significantly decreased ( P 〈 0.01, P 〈 0.05). The levels of NO and NOS were remarkably significantl increased in atorvastatin group( P 〈 0.01, P 〈 0.05). It was ob- served in atorvastatin group that ultrastmctural in aortic endothelial cell were improved. Conclusion : That atorvastatin can cause a significant re- duction in blood pressure in SLIP, is that it may increase the aortic NOS activity and serum NO concentration by decreasing ROS activity and improving endothelial dysfunction.
出处
《皖南医学院学报》
CAS
2008年第4期250-252,共3页
Journal of Wannan Medical College
关键词
阿托伐他汀
高血压
血压
一氧化氮
一氧化氮合
酶
活性氧
大鼠
atorvastatin
hypertensive
blood pressure
nitric oxide
nitric oxide synthase
reactive oxygen species
rats