[Animal modeling] - Establishment of Bama miniature pig hypertension model induced by high-fat and high-salt diet and its mechanism

  Objective: To establish the hypertension model of Bama miniature pig with high-fat and high-salt diet and explore its possible pathogenesis

  Methods: Eighteen male Bama minipigs were randomly divided into three groups: normal control (NC) group, high fat (HF) group and high fat and high salt (HFHS) group, with six pigs in each group. NC group was fed with normal diet, HF group and HFHS group were fed with high fat and high salt diet respectively for 24 weeks. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) of minipigs were measured at 8, 16 and 24 weeks of modeling, and blood glucose, blood lipid and liver and kidney function were measured at 24 weeks of modeling, As well as plasma endothelin-1 (ET-1), renin, angiotensin II (AngII), aquaporin-2 (AQP-2), vasopressin (AVP), vascular endothelial growth factor (VEGF) and other indicators, and take liver and kidney for histopathological observation

  Results: Compared with NC group, SBP and DBP in HF group and HFHS group were significantly higher than those in HF group 8 weeks after modeling, and showed a continuous upward trend; At the same time, after 24 weeks of modeling, the body weight, liver and kidney indexes of small pigs in HF group and HFHS group increased significantly (P<0.05), and the levels of plasma TC, CREA and ET-1 also increased significantly (P<0.05, P<0.01); In the HFHS group, the BUN level decreased significantly (P<0.05), but the contents of renin, Ang ⁃ II, AQP-2, and AVP increased significantly (P<0.05, P<0.01). The oil red "O" staining results showed that the liver and kidney in the HF group and HFHS group had lipid deposition, and renal arteriole wall thickening and other pathological changes

  Conclusion: Hypertension model of miniature pigs can be established after 8-week induction of high-fat and high-salt diet, and its pathogenesis may be related to the influence on renal function and the activation of RAS system and AVP AQP-2