目的 采用高脂高盐饮食建立巴马小型猪高血压模型，并探讨其可能的发病机制。方法 取雄性巴马小型猪18只，随机分成3组：正常对照（NC）组、高脂（HF）组和高脂高盐（HFHS）组，每组6只。NC组饲喂普通饲料，HF组和HFHS组分别饲喂高脂饲料和高脂高盐饲料，连续24周。在造模8周、16周和24周时测量小型猪的收缩压（SBP）和舒张压（DBP），在造模24周时测定血糖血脂和肝肾功能，以及血浆内皮素1（ET-1）、肾素（Renin）、血管紧张素Ⅱ（AngⅡ）、水通道蛋白-2（AQP-2）、血管加压素（AVP）和血管内皮生长因子（VEGF）等指标，并取肝、肾脏进行组织病理学观察。结果 与NC组比，HF组和HFHS组在造模8周后SBP和DBP明显升高，并呈持续上升趋势，且HFHS组高于HF组；同时，造模24周后HF组和HFHS组小型猪的体重和肝、肾脏指数均显著增加（P<0.05），且血浆TC、CREA和ET-1水平亦显著升高（P<0.05, P<0.01）；而HFHS组BUN水平显著降低（P<0.05），但Renin、Ang-II、AQP-2、AVP含量均显著升高（P<0.05，P<0.01）。油红“O”染色结果显示，HF组和HFHS组肝、肾脏出现脂质沉积，且出现肾小动脉管壁增厚等病理改变。结论 高脂高盐饮食诱导8周可建立小型猪高血压模型，其发病机制可能与影响肾脏功能进而激活RAS系统和AVP-AQP-2有关。
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.