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血管紧张素（ＡＮＧ）Ⅱ在１０－１０－１０－６ｍｏｌ／Ｌ范围内剂量依赖性促进无血清培养新生大鼠心肌细胞蛋白质合成速率。蛋白激酶Ｃ（ＰＫＣ）抑制剂ｓｔａｕｒｏｓｐｏｒｉｎｅ（Ｓｔａｕ２ｎｍｏｌ／Ｌ）对心肌细胞基础状态３Ｈ－Ｌｅｕｃｉｎｅ掺入无明显影响，但Ｓｔａｕ预处理３０ｍｉｎ，则可有效阻断ＡＮＧⅡ（１μｍｏｌ／Ｌ）对细胞蛋白质合成的刺激作用；单纯应用ＰＫＣ激活剂ＰＭＡ（１μｍｏｌ／Ｌ）可使心肌细胞蛋白质合成速率增加，与对照组相比，ＰＭＡ组３Ｈ－Ｌｅｕｃｉｎｅ掺入量增加了４１．０４％。细胞Ｎａ＋－Ｈ＋交换抑制剂Ａｍｉｌｏｒｉｄｅ预处理也能阻断ＡＮＧⅡ刺激３Ｈ－Ｌｅｕｃｉｎｅ掺入细胞蛋白质的作用。以上结果提示ＰＫＣ和Ｎａ＋－Ｈ＋交换的激活，可能是ＡＮＧⅡ诱发的心肌细胞肥大反应的重要胞内信息转导机制。本工作还观察到，阻断细胞Ｎａ＋－Ｈ＋交换后并不影响由ＰＫＣ激活导致的蛋白质合成增加，提示可能存在着ＰＫＣ和Ｎａ＋－Ｈ＋交换彼此相对独立地调节心肌细胞生长的途径。
Angiotensin Ⅱ (ANG Ⅱ) promoted the protein synthesis rate of neonatal rat cardiomyocytes in a dose-dependent manner in the range of 10-10-10-6 mol / L. Staurosporine (Stau2nmol / L), a protein kinase C (PKC) inhibitor, had no effect on cardiomyocyte 3H-Leucine incorporation. However, pretreatment with Stau for 30min blocked the effect of ANGⅡ (1μmol / L) on cellular protein synthesis (PMA) alone could increase the rate of protein synthesis in cardiomyocytes. Compared with the control group, 3H-Leucine incorporation in PMA group increased by 41.04%. Pretreatment with Amiloride, a Na + -H + exchange inhibitor, also blocked the effect of ANGII on the incorporation of 3H-Leucine into cellular proteins. The above results suggest that the activation of PKC and Na + -H + exchange may be an important intracellular information transduction mechanism of ANGⅡ-induced cardiomyocyte hypertrophy. This work also observed that blockade of Na + -H + exchange did not affect the increase of protein synthesis induced by PKC activation, suggesting that PKC and Na + -H + exchange may regulate the growth of cardiomyocytes independently of each other.