| Objective To establish a hypertensive model of Bama minipigs using a high-fat and high-salt diet and to explore its mechanism. Methods 18 healthy male Bama minipigs were randomly divided into 3 groups: normal control(NC) group, high-fat(HF) group and high-fat/high-salt(HFHS) group, 6 in each group. The NC group was fed normal basal diet, the HF group and the 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. Minipigs were weighed and the levels of blood glucose, lipids, liver and kidney function as well as endothelin-1 (ET-1), renin, angiotensin II (Ang-II), aquaporin-2 (AQP-2), vasopressin (AVP) and vascular endothelial growth factor (VEGF) levels were determined at 24 weeks after modeling. Meanwhile, the livers and kidneys were taken for histopathological observation. Results Compared with 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 coefficient were significantly increased in the HF and HFHS group (P<0.05), and plasma TC, CREA and ET-1 levels 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 HFHS group were significantly increased (P<0.05, P<0.01). Oil red “O” staining showed that there were lipid deposition in liver and kidney in the HF group and HFHS group, thickening of renal arterial wall and other pathological changes in the HF group and HFHS group. Conclusion Induced by high fat and high salt diet for 8 weeks can establish a hypertensive model of minipigs. Its pathogenesis may be related to the effect of renal function and activation of RAS system and AVP-AQP-2. |