Aim To observe the relationship between the angiotensin Ⅱ Type 1 receptor autoantibody (AT1-AA) and the local inflammation of plaques in atherosclerotic animal model. Methods AT1-AA positive and negative sera were collected and purified from patients with hypertension complicated with acute coronary syndrome. Atherosclerosis models were established in 30 rabbits with hyperlipidemia induced by balloon injury. The animals were randomly divided into 6 groups:(1)control group; (2)low concentration AT1-AA [20 μg/(kg·d)] injection group (LA group); (3)high concentration AT1-AA [40 μg/(kg·d)] injection group (HA group); (4)losartan [20 mg/(kg·d)] lavage＋high concentration AT1-AA injection group (L＋HA group); (5)simvastatin [4 mg/(kg·d)] lavage＋high concentration AT1-AA injection group (S＋HA group); (6)7aa [1.5 mg/(kg·d)] lavage＋high concentration AT1-AA injection group (7aa＋HA group). Each group was treated differently. The abdominal aortas of rabbits were taken out and stained with HE.Image-Pro Express system was used to measure the percentage of atheromatous plaques in the area of lumen. The expressions of MMP-2 in aortic tissue were detected by western blot. Results The values of total cholesterol and low density lipoprotein cholesterol were obviously increased after four weeks. Excluding the control group, the levels of serum AT1-AA in the 8th and 10th week were significantly higher than those at the beginning in the other groups. In LA group and HA group, the relative plaque areas were 46.99%±13.06% and 66.11%±19.67%, respectively, which were significantly higher than those in control group (27.71%±7.46%), L＋HA group (34.27%±12.38%), S＋HA group (24.03%±8.56%) and 7aa＋HA group (28.54%±12.50%) (all P＜0.05). The expressions of MMP-2 in LA group and HA group were significantly higher than those in other groups (all P＜0.05). Conclusion AT1-AA can accelerate the atheromatous plaque formation in rabbit atherosclerosis model and promote the inflammatory reaction and cells proliferation in local plaque.