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氯沙坦减轻自发性高血压大鼠主动脉的血管重塑及其潜在机制。

Losartan attenuates vascular remodeling of the aorta in spontaneously hypertensive rats and the underlying mechanism.

作者信息

Li Fangxiong, Shi Ruizheng, Liao Meichun, Li Jianzhe, Li Shixun, Pan Wei, Yang Tianlun, Zhang Guogang

机构信息

Department of Cardiology, Xiangya Hospital, Central South University, Changsha 410008, China.

出版信息

Zhong Nan Da Xue Xue Bao Yi Xue Ban. 2010 Aug;35(8):807-13. doi: 10.3969/j.issn.1672-7347.2010.08.006.

DOI:10.3969/j.issn.1672-7347.2010.08.006
PMID:20818072
Abstract

OBJECTIVE

To determine the effect of losartan on vascular remodeling and the underlying mechanism in spontaneously hypertensive rats(SHR).

METHODS

SHR of 12 weeks old were given losartan orally [0, 15, 30 mg/(kg.d), n=12]. The tail arterial pressure was measured every week. Eight weeks later, the pathological changes and p22(phox) expression in the thoracic aorta, the activity of catalase (CAT), the contents of H(2)O(2) and Ang II in the plasma were evaluated.

RESULTS

Blood pressure was increased in the SHR accompanied by the thickened wall and increased p22(phox) expression in the thoracic aorta. The plasma levels of H(2)O(2) and Ang II were elevated while the CAT level was decreased in the SHR. Administration of losartan reversed the thickened wall and increased the CAT activity concomitantly with the decreased plasma levels of H(2)O(2) and p22(phox) expression in the SHR. The plasma level of Ang II increased after the losartan treatment.

CONCLUSION

Oxidative stress induces the vascular remodeling of the aorta in the SHR. Losartan can reverse the vascular remodeling through down-regulating p22(phox) expression and inhibiting the oxidative stress.

摘要

目的

确定氯沙坦对自发性高血压大鼠(SHR)血管重塑的影响及其潜在机制。

方法

给12周龄的SHR口服氯沙坦[0、15、30毫克/(千克·天),n = 12]。每周测量尾动脉血压。8周后,评估胸主动脉的病理变化和p22(phox)表达、过氧化氢酶(CAT)活性、血浆中H₂O₂和血管紧张素II的含量。

结果

SHR血压升高,同时胸主动脉壁增厚且p22(phox)表达增加。SHR血浆中H₂O₂和血管紧张素II水平升高,而CAT水平降低。给予氯沙坦可使SHR增厚的血管壁逆转,并增加CAT活性,同时降低血浆中H₂O₂水平和p22(phox)表达。氯沙坦治疗后血浆血管紧张素II水平升高。

结论

氧化应激诱导SHR主动脉血管重塑。氯沙坦可通过下调p22(phox)表达和抑制氧化应激来逆转血管重塑。

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