Objective: To investigate the effect and potential mechanism of chloroquine (CQ) in angiotensin II (AngII) induced murine vascular remodeling. Methods: A total of 32 male C57 BL/6 mice aged 8 weeks were randomly divided into a control group, an AngII group, an AngII + low-dose CQ and an AngII + high-dose CQ (8 mice for each). Control group was left untreated. AngII group received 490 ng/(kg·min) AngII by subcutaneously imbedded osmotic pump. AngII + low-dose and AngII high-dose CQ group were injected intraperitoneally with 10 mg/(kg·d) and 50 mg/(kg·d) CQ respectively based on AngII treatment for 28 days. Mouse blood pressure and heart rate were monitored by using tail-cuff method on day 0, 3, 7, 14, 21 and 28. On day 28, all the mice were sacrificed to collect aortas for H&E and Masson’s staining to access aortic remodeling. Western bolt was performed to detect expression of collagen I/III and autophagy related molecules (LC3B-II and P62). Results: Compared with control group, AngII group presented with elevated blood pressure, thickened aortic vessel wall, significant aortic fibrosis, increased collagen I/III expression, increased autophagic indicator LC3B-II expression and decreased autophagy substance P62. In contrast to AngII group, both low-dose and high dose CQ treatment produced lower blood pressure, thinned aortic vessel, alleviated fibrosis, lowered collagen I/III, more LC3B-II and P62 abundance. Moreover, high-dose CQ treatment showed better improvement than low-dose CQ treatment in terms of all the measurements mentioned above. Conclusion: CQ inhibited AngII induced murine aortic remodeling in a dose dependent manner, which might be mediated through inhibiting over-activated autophagy.