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为研究卡托普利（ＣＡＰ）对心血管组织肾素─血管紧张素系统的影响，５周龄雄性卒中型自发性高血压大鼠（ＳＨＲｓｐ）随机分为实验组（ｎ＝１２）及对照组（ｎ＝８），分别于食管内喂饲ＣＡＰ（６０ｍｇ·ｋｇ－１／ｄ）或蒸馏水，每日１次，持续８周。用放射免疫法测定血浆肾素活性、血管紧张素Ⅱ（ＡｎｇⅡ），心肌和主动脉平滑肌（ＡＳＭ）的肾素浓度（ＲＣ）和ＡｎｇⅡ含量。结果显示，实验组血压不升高，心室重／体重比值也低于对照组；心肌和ＡＳＭ的ＲＣ比对照组高；而ＡｎｇⅡ被明显抑制，分别为７．０２±０．９６比１３．４０±５．３９（Ｐ＜０．０１）和２４．８０±４．９３比３３．６５±８．８９ｐｇ／ｍｇ蛋白（Ｐ＜０．０２）。这说明，ＣＡＰ长期治疗可明显阻止ＳＨＲｓｐ的血压上升及心肌肥厚的发生，降低心肌和ＡＳＭ中ＡｎｇⅡ含量，提示在这种模型，ＣＡＰ降压及抗心肌肥厚的重要机制之一是阻断心血管组织局部ＡｎｇⅡ的生成。
To investigate the effect of captopril on cardiovascular renin-angiotensin system, 5-week-old male stroke spontaneously hypertensive rats (SHRsp) were randomly divided into experimental group (n = 12) and control (N = 8) were fed with esophageal CAP (60 mg · kg-1 / d) or distilled water once daily for 8 weeks. Plasma renin activity, angiotensin II (AngⅡ), renin concentration (RC) and AngⅡ in myocardium and aortic smooth muscle (ASM) were measured by radioimmunoassay. The results showed that the experimental group did not increase the blood pressure, ventricular weight / body weight ratio was lower than the control group; myocardial RCM and ASM higher than the control group; Ang Ⅱ was significantly inhibited, respectively 7.02 ± 0.96 than 13.40 ± 5.39 (P <0.01) and 24.80 ± 4.93 vs. 33.65 ± 8.89 pg / mg protein (P <0.02). This shows that long-term CAP treatment can significantly prevent SHRsp blood pressure and cardiac hypertrophy, reduce myocardial and ASM Ang Ⅱ content, suggesting that in this model, CAP antihypertensive and anti-hypertrophy, one of the important mechanisms to block the cardiovascular Formation of local Ang II.