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Objective To investigate the role of proline-rich protein tyrosine kinase (Pyk2) in angiotensin Ⅱ(Ang Ⅱ)-induced cardiac hypertrophy and the underlying mechanism in rat. Methods Primary rat cardio-myocytes were isolated from rats and randomly divided into control group, Ang Ⅱ induction group (the dose of Ang Ⅱ was 100 nmol/L, cardiomyocytes were stimulated in the cell culture dish for 24 hours), Pyk2 inhibitor PF-431396 group (the dose of PF-431396 was 10 μmol/L, added to the cell culture dish 30 minutes in advance before Ang Ⅱ stimulation) and Ang Ⅱ induction group intervened by PF-431396 (the dose of Ang Ⅱ was 100 nmol/L, the dose of PF-431396 was 10 μmol/L). The size of cardiomyocytes was measured by α-actinin fluorescence staining. RT-qPCR was performed to detect the mRNA level of hypertrophic markers (ANP and β-MHC) in cardiomyocytes. The expressions of p-Pyk2, Pyk2 and p53 in cardiomyocytes were detected by Western blot analysis. Results Ang Ⅱ stimulation increased the surface area of cardiomyocytes and the mRNA level of hypertrophic markers(P＜0.05). In addition, the proteins of p-Pyk2 and p53 were increased(P＜0.05). However, after treatment of Pyk2 inhibitor PF-431396, moycardial hypertrophy was significantly improved and the protein level of Pyk2 and p53 decreased(P＜0.05). Conclusions Pyk2 promotes cardiomyocyte hypertrophy in rat induced by Ang Ⅱ through the p53 signaling pathway.