血管紧张素2型受体在接受雌二醇治疗的去卵巢大鼠中对给予血管紧张素II时一氧化氮产生反应的作用
Role of Angiotensin Type 2 Receptor on Nitric Oxide Production Response to Angiotensin II Administration in Ovariectomised Rats Treated with Estradiol.
作者信息
Safari Tahereh, Nematbakhsh Mehdi
机构信息
Department of Physiology, Zahedan University of Medical Sciences, Zahedan, Iran.
Water and Electrolytes Research Center, Isfahan University of Medical Sciences, Isfahan, Iran ; Department of Physiology, Isfahan University of Medical Sciences, Isfahan, Iran ; Isfahan Institute of Basic and Applied Sciences Research, Isfahan, Iran.
出版信息
Int J Prev Med. 2014 Feb;5(2):238-40.
BACKGROUND
Renin-angiotensin system activity is gender related. The vasodilatory response of angiotensin II (AngII) angiotensin type 2 receptor (AT2R) may involve nitric oxide (NO) production. We attempted to find the role of AT2R on NO formation response to AngII administration in ovariectomised rats treated with estradiol (OVE).
METHODS
A total of 33 female Wistar rats were divided into 3 groups; intact animals, ovariectomised treated with placebo (OVX) and OVE. At 2 weeks later, all animals were subjected to anesthetize and catheterize and each group was divided into two subgroups that received AT2R antagonist (PD123319) or vehicle. Each animal was subjected to 1 h continuous infusion of AngII (~20 μg/kg/h) and the level of NO metabolite (nitrite) was measured before and after AngII infusion.
RESULTS
At the presence of AT2R, the serum level of nitrite in response to AngII administration in OVE groups increased significantly (P < 0.05).
CONCLUSIONS
However, this increase was abolished by AT2R antagonist. It seems that AT2R involves nitrite production response to AngII in OVE.
背景
肾素 - 血管紧张素系统活性与性别相关。血管紧张素II（AngII）血管紧张素2型受体（AT2R）的血管舒张反应可能涉及一氧化氮（NO）的产生。我们试图探究AT2R在用雌二醇治疗的去卵巢大鼠（OVE）中对AngII给药时NO形成反应的作用。
方法
总共33只雌性Wistar大鼠被分为3组；完整动物组、用安慰剂治疗的去卵巢组（OVX）和OVE组。2周后，所有动物接受麻醉和插管，每组再分为接受AT2R拮抗剂（PD123319）或赋形剂的两个亚组。每只动物接受1小时持续输注AngII（约20μg/kg/h），并在AngII输注前后测量NO代谢物（亚硝酸盐）水平。
结果
在存在AT2R的情况下，OVE组中对AngII给药的亚硝酸盐血清水平显著升高（P < 0.05）。
结论
然而，这种升高被AT2R拮抗剂消除。似乎AT2R参与了OVE中对AngII的亚硝酸盐产生反应。
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