目的探讨钙调神经磷酸酶（ＣａＮ）依赖的信号通路在血管紧张素Ⅱ（ＡｎｇⅡ）刺激的乳鼠心肌成纤维细胞（ＦＢｓ）增殖中的作用。方法以培养的ＦＢｓ为模型，用ＡｎｇⅡ刺激ＦＢｓ外Ｃａ２＋入流，环抱素Ａ（ＣｓＡ）阻断ＣａＮ信号通路，维拉帕米（Ｖｅｒ）阻断ＦＢｓ钙通道，检测ＦＢｓ　ＣａＮ、丝裂素活化蛋白激酶（ＭＡＰＫ）、蛋白激酶 Ｃ（ＰＫＣ）活性，用［３Ｈ］－亮氨酸及［３Ｈ］－胸腺嘧啶参入量作为反应 ＦＢｓ增殖的指标。结果Ａｕｇ Ⅱ刺激组ＦＢｓ蛋白核酸合成速率明显增高，与对照组相比差异有显著性（Ｐ＜０．０１）；ＣｓＡ及Ｖｅｒ能明显抑制Ａｎｇ Ⅱ介导的ＦＢｓ蛋白核酸合成速率增高，与ＡｎｇⅡ血刺激组相比差异有显著性（ Ｐ＜ ０． ０１）。同时发现 Ａｎｇ Ⅱ刺激组 ＣａＮ、ＰＫＣ活性与对照 ＦＢｓ相比差异有显著性（ Ｐ＜ ０． ０５或 Ｐ＜０．０１）。 ＣｓＡ和Ｖｅｒ抑制ＡｎｇⅡ介导的 ＦＢｓ ＣａＮ活性增高，Ｖｅｒ抑制Ａｎｇ Ⅱ介导的ＦＢｓＰＫＣ活性的增高。结论 ＣａＮ信号通路在ＡｎｇⅡ刺激的ＦＢｓ增殖中起重要作用，但ＣａＮ信号通路不是ＡｎｇⅡ介导ＦＢｓ的增殖的唯一信号通路，以ＭＡＰＫ为核心的信号通路亦参与了ＡｎｇⅡ刺激的ＦＢｓ增殖。 Objective To investigate the role of calcineurin (CaN) -dependent signaling pathway in the proliferation of neonatal rat cardiac fibroblasts (FBs) stimulated with angiotensin Ⅱ (AngⅡ). Methods The cultured FBs were used as the model. The Ca2 + influx was detected by Ang Ⅱ stimulation. CsA blocked the CaN signaling pathway. Verapamil blocked the calcium channels of FBs, detected the expression of Ca2 +, mitogen-activated protein MAPK and PKC, and the [3H] -leucine and [3H] -thymidine incorporation were used as indexes for the proliferation of FBs. Results The mRNA synthesis rates of FBs in Aug Ⅱ stimulated group were significantly higher than those in control group (P <0.01). CsA and Ver significantly inhibited Ang Ⅱ -mediated FBs protein synthesis, Blood stimulation group compared with the difference was significant (P <0.01). Also found that Ang Ⅱ stimulation group CaN, PKC activity compared with the control FBs was significantly different (P <0.05 or P <0.01). CsA and Ver inhibited the AngⅡ-mediated increase of CaN activity in FBs and Ver inhibited the increase of Ang Ⅱ-mediated FBsPKC activity. Conclusions CaN signaling pathway plays an important role in the proliferation of FBs stimulated by AngⅡ. However, CaN signaling pathway is not the only signal pathway that Ang Ⅱ mediates the proliferation of FBs. MAPK signaling pathway is also involved in the proliferation of FBs stimulated by AngⅡ.