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中国临床药理学与治疗学 ›› 2005, Vol. 10 ›› Issue (6): 682-686.

• 研究原著 • 上一篇    下一篇

血管紧张素受体阻滞剂对自发性高血压大鼠肾脏血管紧张素转换酶2表达的影响

杨柳, 刘昌慧, 王毅, 白玉鹏   

  1. 武汉大学人民医院老年病科, 武汉430060, 湖北
  • 收稿日期:2005-04-01 修回日期:2005-06-02 出版日期:2005-06-26 发布日期:2020-11-12
  • 通讯作者: 刘昌慧, 女, 教授, 主任医师, 硕士生导师, 研究方向:老年心血管疾病。Tel:027-88041919-2906 E-mail: changhuiliu65@yahoo.com.cn
  • 作者简介:杨柳, 女, 硕士研究生, 研究方向:老年心血管病。Tel:027-87377728 E-mail: yanglulu999@hotmail.com

Effects of angiotensin type-1 receptor blockade on expression of angiotensin-converting enzyme 2 in renal of spontaneously hypertensive rats

YANG Liu, LIU Chang-hui, WANG Yi, BAI Yu-peng   

  1. Department of Geriatrics, Renming Hospital of Wuhan University, Wuhan 430060, Hunan, China
  • Received:2005-04-01 Revised:2005-06-02 Online:2005-06-26 Published:2020-11-12

摘要: 目的: 研究自发性高血压大鼠肾脏血管紧张素转换酶2(ACE2) 蛋白表达水平及血管紧张素Ⅱ-Ⅰ型受体阻滞剂厄贝沙坦对ACE2表达的影响, 以了解高血压的病理改变, 探讨血管紧张素受体阻滞剂治疗高血压又一可能机制。方法: 20 只14 周龄雄性自发性高血压大鼠随机分为自发性高血压大鼠(SHR) 组(n =10) 和厄贝沙坦组(n =10) 。厄贝沙坦组每只大鼠以厄贝沙坦50 mg·kg-1·d-1灌胃, 给药时间12 周。同时取14 周龄雄性京都种Wistar 大鼠为正常对照(WKY) 组(n =10) 。利用免疫组化和逆转录聚合酶链反应检测各组大鼠肾脏ACE2 表达。结果: 与WKY 组比较, SHR 组ACE2 表达显著减少(0.72 ±0.11 vs 1.11 ±0.15); 与SHR 组比较, 厄贝沙坦组经12 周治疗后, ACE2 表达明显提高(1.03 ±0.13 vs 0.72 ±0.11) 。结论: 高血压大鼠肾脏ACE2表达减少, 血管紧张素Ⅱ-Ⅰ 型受体阻滞剂对高血压大鼠肾脏ACE2 的表达有上调作用。此作用可能是血管紧张素受体阻滞除阻滞血管紧张素受体以外的另一间接调节肾素-血管紧张素系统的途径。

关键词: 自发性高血压大鼠, 血管紧张素转换酶2, 肾脏, 血管紧张素II, 厄贝沙坦

Abstract: AIM: To investigate the expression of angiotensin-converting enzyme 2 (ACE2) in the renal of spontaneously hypertensive rats and the effects of angiotensin type-1 receptor blockade. METHODS: Twenty of 14-week-old male SHR were randomly divided into two groups (n =10 in each): SHR group and irbesartan group. Ten of 14-week-old male WKY group were served as control. Irbesartan group were given a daily dose of 50 mg·kg-1 irbesartan for 12 weeks by gavage and the other two groups were fed with a normal diet. Angiotensin-converting enzyme 2 was examined by immunohistochemistry and RT-PCR. RESULTS: ACE2 in the renal was significantly down-regulated in the SHR group compared with the WKY group (0.72 ±0.11 vs 1.11 ±0.15). After 12 weeks treatment with irbesartan, the attenuated ACE2 expression in irbesartan group was markedly enhanced compared with the SHR group (1.03 ±0.13 vs 0.72 ± 0.11). CONCLUSION: Hypertension induces the reduction of ACE2 in the renal in rats and irbesartan markedly increases ACE2 expression. It suggests that up-regulation ACE2 which is one of counter-regulatory particular components in the renin-angiotensin system may be a new mechanism of curing hypertension beyond blockade angiotensin type-1 receptor.

Key words: spontaneously hypertensive rat, angiotensin-converting enzyme 2, renal, angiotensinII, irbesartan

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