Objective To establish a Bama minipig model of hypertension induced by high?fat and high?salt diet and to explore its mechanism. Methods Eighteen healthy male Bama minipigs were randomly divided into 3 groups: normal control (NC) group, high?fat (HF) diet group and high?fat/ high?salt diet (HFHS) group, 6 in each group. The NC group was fed normal basal diet, the HF group and HFHS group were fed with high?fat diet and high?fat/ high?salt diet for 24 weeks, respectively. The systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured at 8, 16 and 24 weeks of modeling. The minipigs were weighed and the levels of blood glucose, lipids, liver and kidney function as well as the levels of endothelin - 1 (ET - 1), renin, angiotensin II (Ang?II), aquaporin - 2 (AQP - 2), vasopressin (AVP) and vascular endothelial growth factor (VEGF) were determined at 24 weeks after modeling. Meanwhile, samples of liver and kidney tissues were taken for histopathological examination. Results Compared with the NC group, SBP and DBP were significantly increased in the HF and HFHS groups after 8 weeks of modeling and showed a continuous rising trend, and the HFHS group was higher than that in the HF group. The body weight and liver and kidney coefficients were significantly increased in the HF and HFHS groups ( P < 0. 05), and levels of plasma TC, CREA and ET - 1 were significantly increased ( P < 0. 05, P < 0. 01). In addition, the level of BUN was significantly decreased ( P < 0. 05) and the levels of renin, Ang?II, AQP - 2 and AVP in the HFHS group were significantly increased ( P < 0. 05, P <0. 01). Oil red “O” staining showed lipid deposition in the liver and kidney tissues, and thickening of renal arterial wall and other pathological changes in the HF and HFHS groups. Conclusions A Bama minipig model of hypertension is successfully established by high fat and high salt diet for 8 weeks. Its pathogenesis may be related to the effect of alteration in renal function and activation of RAS system and AVP?AQP -2.