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目的:观察氯沙坦治疗对自发性高血压大鼠(SHR)主动脉重构及p22phox表达的影响。方法:36只12周龄SHR连续灌胃给予氯沙坦,剂量分别为0,15,30 mg/(kg.d),每组12只;另取12只WKY大鼠作为非高血压对照组。每周测定尾动脉压。8周后检测主动脉病理结构、血浆过氧化氢(H2O2)水平、过氧化氢酶(CAT)活力、血浆血管紧张素Ⅱ(Ang II)水平、主动脉p22phox的表达。结果:SHR主动脉血管壁明显增厚,尾动脉压、血浆H2O2和AngⅡ水平及主动脉p22phox的表达均显著增高,而血浆CAT活力明显下降;应用氯沙坦治疗在降低血压的同时,可改善SHRL主动脉结构,降低血浆H2O2水平和主动脉p22phox的表达,升高血浆AngⅡ水平及和CAT活力。结论:SHR主动脉血管重构涉及氧化应激,氯沙坦可改善血管重构,其机制与下调p22phox表达、抑制氧化应激有关。
Objective: To observe the effect of losartan on aortic remodeling and p22phox expression in spontaneously hypertensive rats (SHR). METHODS: Thirty-six SHRs of 12 weeks old were given continuous intragastric administration of losartan at doses of 0, 15 and 30 mg / (kg.d), with 12 rats in each group. Another 12 WKY rats were used as non-hypertension control group . Tail arterial pressure was measured weekly. After 8 weeks, the pathological structure of the aorta, plasma H2O2 level, catalase (CAT) activity, plasma angiotensin Ⅱ (Ang II) level and aorta p22phox expression were detected. Results: The aortic wall of SHR was significantly thicker, the tail arterial pressure, plasma H2O2 and AngⅡ levels and aortic p22phox expression were significantly increased, while the plasma CAT activity was significantly decreased; losartan treatment can reduce blood pressure at the same time, can improve SHRL aortic structure, reducing plasma H2O2 levels and aortic p22phox expression, increased plasma Ang Ⅱ levels and CAT activity. CONCLUSIONS: Aortic vascular remodeling in SHR involves oxidative stress. Losartan improves vascular remodeling. Its mechanism is related to down-regulation of p22phox and inhibition of oxidative stress.