AngⅡin paraventricular nucleus contribute to chronic intermittent hypoxia induced-hypertension in rats

Xiaohai YU; Yan LI; Yang Ding; Zhiqiang Tang; Jinli Wang; Yifei Fan; Wenhui Cheng; Mingkui Zhong

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AngⅡin paraventricular nucleus contribute to chronic intermittent hypoxia induced-hypertension in rats

VernacularTitle:室旁核血管紧张素Ⅱ在慢性间歇性低氧诱发大鼠高血压中的作用及机制
Author: Xiaohai YU ; Yan LI ; Yang DING ; Zhiqiang TANG ; Jinli WANG ; Yifei FAN ; Wenhui CHENG ; Mingkui ZHONG
Publication Type:Journal Article
Keywords: paraventricular nucleus; angiotensin Ⅱ; chronic intermittent hypoxia; systolic blood pressure; hypertension; Ang Ⅱ type 1 receptor
From: Chinese Pharmacological Bulletin 2015;(5):716-720
CountryChina
Language:Chinese
Abstract: Aim To determine whether AngⅡin para-ventricular nucleus (PVN)was involved in the chronic intermittent hypoxia (CIH ) induced-hypertension in rats.Methods Male Sprague-Dawley rats were ran-domly divided into Sham and CIH groups,the Sham rats were exposed to continuous normoxia,while the CIH rats were submitted to CIH (8 h per day for 15 days).The conscious noninvasive method with tail cuff was performed in rats to record the systolic blood pres-sure during establishing the model of CIH induced hy-pertension.Mean arterial pressure (MAP)and heart rate (HR)were recorded in vivo on a PowerLab data acquisition system after CIH.Rats were fixed on the stereotaxic instrument to conduct microinjection in the PVN.We used Western blot to measure Ang Ⅱ level and AngⅡtype 1 receptor (AT1 R)protein expression in PVN.Results The level of PVN Ang Ⅱin CIH rats was significantly higher than that in Sham rats,a-long with increased AT1 R protein expression.Microin-jection of Ang Ⅱ(0.03,0.3,3 nmol)in bilateral PVN dose-dependently increased MAP in both CIH and Sham rats,and this response was significantly augmen-ted in CIH rats.Losartan (50 nmol),AT1 R antago-nist,had no effect on MAP in Sham rats,but caused significant MAP decreases in CIH rats,and prevented Ang Ⅱ-induced increases in MAP in both CIH and Sham rats.Conclusion The results suggest that the increased AngⅡrelease and enhanced AT1 R activation in the PVN contribute to CIH induced-hypertension in rats.