Aim To research the role of adiponectin（APN）in hypertension-induced cardiac inflammation and fibrosis.Methods Select 12 homozygous adiponectin knockout mice（APN^-/-） and 12 wild-type mice （WT） to establish the hypertension model by using the trace of continuous infusion pump angiotensin Ⅱ （AngⅡ） （1500 ng·min,7 d）,and the control group was given the trace of pump infusion acetic acid solution and for 7 days. The experiment is divided into four groups at random: the control group of wild-type mice （WT,6）,+ angiotensin Ⅱ group of wild type mice （WT + AngⅡ,6）,APN^-/- in the control group （APN^-/-,6）,APN^-/- + angiotensin Ⅱ （APN^-/- + AngⅡ ,6）,using noninvasive blood to pressure mice tail artery blood pressure,detecting the content of sICAM 1,sVCAM 1 and vWF in serum by using the method of ELISA. Myocardial tissue masson staining was used to observe cardiac fibrosis,α-SMA immunohistochemical method to observe the formation of muscle fibroblasts,HE staining to observe the inflammatory cells infiltration,western blot method to measure TGF-β,TNF-α protein expression.Results Compared with WT group,the blood pressure of WT + AngⅡ group begins to rise at the next day ,and the blood pressure increases obviously （P<0.05） for seven consecutive days,which explains that the building is successful. Compared with WT + AngⅡ group,the blood pressure of APN^-/- + AngⅡ group increases obviously （P<0.05）,inflammatory cells infiltration increases obviously （P<0.05）,the content of sICAM 1,sVCAM 1,vWF increases obviously,the expression of TGF-β and TNF-α is upregulated obviously,α-SMA + muscle fibroblast populations increase （P<0.05）.Conclusion In the process of high blood pressure caused by cardiac fibrosis,adiponectin maybe protect vasc ular endothelium injury,inhibiting inflammatory reaction,thereby inhibiting cardiac fibrosis.