Establishment of a model of hypertension in Bama mini-pigs induced by high-fat and high-salt diet and its mechanism

  Objective: To establish a Bama mini-pig hypertension model with a high-fat and high-salt diet and explore its possible pathogenesis. Method: Take 18 male Bama miniature pigs and randomly divide them into 3 groups: normal control (NC) group, high-fat (HF) group and high-fat and high-salt (HFHS) group, each with 6 pigs. NC group is fed with ordinary feed , HF group and HFHS group were fed high-fat diet and high-fat high-salt diet for 24 consecutive weeks. The systolic blood pressure (SBP) and diastolic blood pressure (DBP) of the miniature pigs were measured at 8 weeks, 16 weeks and 24 weeks after modeling. Measure blood glucose, blood lipids, liver and kidney function, and plasma endothelin 1 (ET-1), renin (Renin), angiotensin II (AngII), and aquaporin-2 (AQP-2) at 24 weeks after modeling 、 Vasopressin (AVP) and vascular endothelial growth factor (VEGF) and other indicators, and take liver and kidney for histopathological observation. Results: Compared with the NC group, the SBP and DBP of the HF group and the HFHS group increased significantly after 8 weeks of modeling, and showed a continuous upward trend, and the HFHS group was higher than the HF group; at the same time, the HF group and HFHS group 24 weeks after the modeling The body weight and liver and kidney indexes of the miniature pigs in the group increased significantly (P<0.05), and the plasma TC, CREA and ET-1 levels were also significantly increased (P<0.05, P<0.01); while the BUN level of the HFHS group was significantly reduced (P<0.05), but the contents of renin, Ang-II, AQP-2, and AVP were significantly increased (P<0.05, P<0.01). The oil red "O" staining results showed that the liver and kidney of the HF group and the HFHS group There are lipid deposits and pathological changes such as thickening of the renal arterioles.

   Conclusion: High-fat and high-salt diet can be induced for 8 weeks to establish a mini-pig hypertension model, and its pathogenesis may be related to affecting kidney function and activating the RAS system and AVP-AQP-2.