Abstract: Objective To study the effect of apelin-13 on myocardial fibrosis in hypertensive rats and its underlying mechanism. Methods Forty male Sprague Dawley (SD) rats aged 8 weeks were randomly divided into AAC group (n=32) and sham operation group (n=8). After modeling the survival, the rats were randomly divided into three groups: apelin-13 group (n=8), valsartan VST group (n=8) and model group (n=8). The effect of apelin-13 on their cardiac function status and hemodynamical indexes were tested. ELISA kit was used to measure the concentration of AngⅡand Ang (1-7) in blood; Expression level of signaling pathways related protein TGF-β1, TIMP, PAI-1 and MMP-2 were detected by Western-blotting; Morphology of collagen in myocardial tissue was observed by HE and Masson staining, collagen volume fraction (CVF) in left ventricular interstitial tissue was measured by image analysis. Results The cardiac function of AAC group decreased significantly compared with the sham operation group, apelin-13 group and VST group (P< 0.05), and VST group was lower than apelin-13 group. Compared with the drug treatment group, the serum levels of Ang-(1-7) in ACC group decreased while the serum levels of Ang (Ⅱ) increased (P< 0.05), and no statistically significant difference was found between apelin-13 group and VST group (P> 0.05). The CVF in left ventricular interstitial tissue, and the TGF-β1, TIMP, PAI-1 protein expression levels were significantly higher whereas the MMP-2 expression level was significantly lower in apelin-13 group, VST group and ACC group than in sham operation group (P< 0.05), and both drug treatment groups were significantly lower than AAC group with apelin-13 group lower than VST group (P< 0.05). Conclusion Apelin-13 can improve myocardial fibrosis in hypertensive rats by inhibiting the renin - angiotensin - aldosterone system, thereby inhibiting the expression of TGF-β1, PAI-1, TIMP-1 and improving the expression of MMP-2.