心肌细胞自分泌的血管紧张素Ⅱ在心肌肥厚中的作用

The role of angiotensin Ⅱ released from cardiac myocytes in the hypertrophic response

目的：探讨心肌细胞自分泌的血管紧张素Ⅱ在心肌肥厚中的作用。方法：应用体外心肌细胞肥厚模型，采用放免法观察心肌肥厚时，心肌细胞自分泌的血管紧张素Ⅱ的变化；并应用３Ｈ－亮氨酸掺入法测定血管紧张素Ⅱ对培养的心肌细胞蛋白合成的改变。结果：机械牵拉体外培养的心肌细胞在引起心肌细胞肥厚的同时，心肌细胞血管紧张素Ⅱ的自分泌增加。血管紧张素Ⅱ作用于培养的心肌细胞可引起其蛋白合成的增加；而同时加入血管紧张素Ⅱ受体特异性拮抗剂［Ｓａｒ１，Ｉｌｅ８］－Ａｎ－ｇｉｏｔｅｎｓｅⅡ（ＳＡＲ）后，则可抑制必要的合成。结论：心肌细胞自分泌的血管紧张素Ⅱ在心肌肥厚的形成中起着重要的作用。

Objective: To study the significance of angiotensin Ⅱ(Ang Ⅱ) released from cardiac myocytes in the hypertrophic response. Methods: A model of cardiac hypertrophy in vitro was used in this study. The level of Ang Ⅱ autocrine released from the hypertrophic cardiac myocytes was quantitatively determined by radioimmunoassay. The protein synthesis of the cultured cardiac myocytes to Ang Ⅱ was examined by 3Hleucine incorporation. Results: Stretching the cultured myocardial cells by mechanical force in vitro, caused an increase of Ang Ⅱ released from cardiac myocytes, as well as the hypertrophic response of the cardiac myocytes. Ang Ⅱ stimulated protein synthesis in cultured myocytes. But in the presence of [Sar1,Ile8]Ang Ⅱ(SAR), a specific Ang Ⅱ receptor antagonist, this hypertrophic response was suppressed. Conclusion: Ang Ⅱ released from cardiac myocytes plays a critical role in the hypertrophic response.