Aim To observe the effect of putative receptor protein related to the angiotensin receptor AT1 (APJ) agonist Apelin-13 on the hypertensive renal fibrosis and to explore the possible mechanism in spontaneously hypertensive rat (SHR). Methods Male SHRs of 12 weeks old were randomly divided into control group and 1 μg/(kg·d) Apelin-13 group, 10 μg/(kg·d) Apelin-13 group, 100 μg/(kg·d) Apelin-13 group. The rats were administrated with Apelin-13 by tail vein for 12 weeks. 24 h urine protein was continuously measured. Serum creatinine and urea nitrogen were measured. Systolic blood pressure (SBP) was continuously measured by tail method. Histological change of kidney was observed by HE staining and Masson staining. The expressions of autophagy related protein microtubule-associated protein light chain-3 (LC3), Beclin-1 and the autophagy substrates p62 in the kidney were determined by Western blot. Results Compared with control group, SBP, 24 h urine protein, serum creatinine and urea nitrogen, renal injury score and collagen volume fraction were significantly decreased in dose-dependent manner in 10 μg/(kg·d) Apelin-13 group and 100 μg/(kg·d) Apelin-13 group (all P<0.05). The edema of renal tubular epithelial cells was alleviated, the interstitial collagen deposition was decreased, and the degree of renal interstitial fibrosis was decreased in 10 μg/(kg·d) Apelin-13 group and 100 μg/(kg·d) Apelin-13 group. Compared with control group, LC3-Ⅱ expression, LC3-Ⅱ/LC3-Ⅰ ratio and Beclin-1 expression were singificantly increased and p62 expression was singificantly decreased in kidney in dose-dependent manner in 10 μg/(kg·d) Apelin-13 group and 100 μg/(kg·d) Apelin-13 group (all P<0.05). Conclusion Apelin-13 inhibits the progression of hypertensive renal fibrosis, and its mechanism may be related to the inhibition of autophagy by Apelin-13.