摘要
目的 研究福辛普利和氯沙坦对自发性高血压大鼠 (SHR)血管紧张素Ⅱ受体 1(AT1 R)的基因表达水平及心血管细胞增殖的影响 ,探讨高血压病的病理机制。方法 48只 10周龄SHR随机分 3组 ,1组 :服福辛普利 5mg·kg-1·d-1;2组 :服氯沙坦 2 0mg·kg-1·d-1;3组 (对照组 ) :服安慰剂。 3组分别灌胃持续 9周 ,实验前及实验中每 2周测尾动脉血压 ,9周后 ,抽血并处死动物取材 ,放免法测血管紧张素Ⅱ (AngⅡ ) ,用半定量RT PCR测量心肌AT1 R的mRNA水平 ,光、电镜观察心肌及主动脉组织学改变。 结果 血压 :对照组随增龄上升 ,两治疗组实验第 2周起各次均较治疗前低 ,差异多具显著性 ,实验第 8周福辛普利组为 (16 5 .1± 4 9)mmHg、氯沙坦组为 (15 6 3± 4 2 )mmHg ,均较对照组 (179 1± 10 4 )mmHg低 ,差异显著 ,P <0 0 1。血浆AngⅡ浓度 :对照组为 (4 40 0± 190 3) pg/mL ,福辛普利组为 (5 6 6 0± 149 3) pg/mL和氯沙坦组 (5 2 9 3± 2 0 0 9)pg/mL均较对照组高 ,但均无显著性差异 ,P >0 0 5。心肌AT1 R的mRNA水平 :福辛普利组为 (72 0± 35 0 ) %,对照组为 (10 2 4± 2 1 9) %,显著高于前者 ,P <0 0 5 ;氯沙坦组为 (10 1 9± 2 7 3) %,与对照组差异无显著性 ,P >0 0 5 ,但较福辛普利组高 。
Objective To study the effect of fosinpril(Fos) and losartan(Los) on angiotensin Ⅱ receptor1(AT 1-R) gene expression in myocardium in SHR. Methods Forty-eight 10 wk old SHR were divided randomly into 3 groups:Fos treated group(5 mg·kg -1·d -1);Los treated group(20 mg·kg -1·d -1),and control. Medications were fed through gastric gavage for 9 wks. BP was measured using tail-cuff methods every 2 wks. After 9 wks treatment,blood and total RNA were extracted from the myocardium of SHR. Plasma Ang Ⅱ were measured with radioimmunoassay. The mRNA of myocardium AT 1-R were measured with RT-PCR. Histology study of the mycardium and aorta was examined using light microscope and electromicroscope. Results Fos and Los decreased BP significantly from 2nd wk of treatment. At the 8th wk,BP in Fos group was 165±5 mmHg,Los group was 179±10 mmHg,and control group was 179±10 mmHg. No difference of plasma AngⅡ level was found among the 3 groups. The mRNA level of myocardium AT 1-R was (72±35)% in Fos group,(102±27)% in Los group and (102±21)% in control. mRNA of AT 1-R was signficantly lower in Fos group than that in control(P<0.05) with little difference between Los group and control. Both Fos and Los treatment significantly alleviated cardiovascular cell hypertrophy with better effects found in Los. Conclusion The gene expression of myocardium AT 1-R in SHR was attenuated by Fos but not by Los. Although both of them inhibited the development of cardiovascular hypertrophy.
出处
《高血压杂志》
CSCD
2002年第4期356-361,共6页
Chinese Journal of Hypertension
基金
深圳市三项科技经费资助 (编号 :19980 5 0 4)
