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目的研究压力负荷产生的心肌肥厚过程中的肾素－血管紧张素系统（ＲＡＳ）作用。方法应用ｌｏｓａｒｔａｎ（Ｌｏｓ）及卡托普利（Ｃａｐ）研究心肌ＲＡＳ在压力超荷大鼠心肌肥厚中的作用。狭窄大鼠腹主动脉造成压力超荷（ＣｏＡ），术后第二天给予ＣｏＡ大鼠亚降压量Ｌｏｓ（３ｍｇ／ｋｇ·ｄ－１）与Ｃａｐ（３０ｍｇ／ｋｇ·ｄ－１）。结果不影响动脉血压，但左室重分别减少５８．３％及６２．５％，左室／体重比值显著低于ＣｏＡ组（４．１２±０．１７及３．９２±０．２３ｖｓ４．８６±０．１８，Ｐ＜０．０５），但左室重与假手术组比仍有差异。高血压肥厚２周大鼠，经亚降压量Ｌｏｓ及Ｃａｐ治疗２周后，左室重较治疗前分别减少６０％及６４％，蛋白质含量显著低于ＣｏＡ组（１０２．１±１４及９８．５±１５ｍｇｖｓ１４３．３±１９ｍｇ，Ｐ＜０．０５），但高于正常组。结论Ｌｏｓ与Ｃａｐ逆转肥厚的机制除降压外，阻断心肌ＲＡＳ活性起重要作用
Objective To investigate the effect of renin-angiotensin system (RAS) during cardiac hypertrophy induced by pressure overload. Methods Losartan (Los) and captopril (Cap) were used to study the role of myocardial RAS in cardiac hypertrophy induced by pressure overload in rats. Pressure overload (CoA) was induced in the abdominal aorta of stenosed rats, and Los (3 mg / kg · d-1) and Cap (30 mg / kg · d-1) were given to CoA rats the day after the operation. The results did not affect arterial blood pressure, but left ventricular mass decreased by 58.3% and 62.5%, respectively, and left ventricular mass / body weight ratio was significantly lower than those in CoA group (4.12 ± 0.17 and 3.92 ± 0.23 vs 4.86 ± 0.18, P <0.05), but there was still a significant difference between left ventricular weight and sham group. Hypertensive hypertrophy in 2 weeks of rats, sub-reduced pressure Los and Cap after 2 weeks of treatment, the left ventricular weight was reduced by 60% and 64% compared with before treatment, the protein content was significantly lower than the CoA group (102.1 ± 14 and 98 .5 ± 15 mg vs 143.3 ± 19 mg, P <0.05), but higher than the normal group. Conclusion The mechanism of Los and Cap reversal of hypertrophy, in addition to antihypertensive, block the myocardial RAS activity plays an important role