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目的：探讨压力超负荷致心肌肥大的跨膜信号传递机制。方法：利用放射免疫法及分光光度法动态观察压力超负荷后大鼠心肌组织血管紧张素转换角活性，血管紧张素Ⅱ、内皮索和一氧化氢含量的变化，并观察它们与压力超负荷心肌肥大的关系。结果：随大鼠动脉血压逐步升高，心肌组织中血管紧张素转换酶活性，血管紧张素Ⅱ、内皮素含量均迅速升高（P＜0．05），并持续保持高水平，血管紧张素Ⅱ升高早于内皮系，而一氧化氛含量迅速降低并持续受抑（P＜0．05）。结论：心肌内分泌活化可能是介导压力超负荷致心肌肥大的重要机制。
Objective: To investigate the transmembrane signal transduction mechanism of hypertrophy induced by pressure overload. Methods: The changes of Angiotensin Converting Angiotensin Ⅱ activity, angiotensin Ⅱ, endothelium and hydrogen peroxide in myocardium were observed by radioimmunoassay and spectrophotometry. The changes of angiotensin Ⅱ, Hypertensive relationship. Results: With the gradual increase of arterial blood pressure in rats, the contents of angiotensin Ⅱ and endothelin in the myocardium increased rapidly (P <0.05) and maintained high levels of angiotensin Ⅱ increased earlier than that of the endothelium, while the content of the oxidant decreased rapidly and persisted (P <0.05). Conclusion: Myocardial endocrine activation may be an important mechanism to mediate pressure overload induced hypertrophy.