中文摘要：

目的 研究室旁核（PVN）中血管紧张素Ⅱ（AngⅡ）-活性氧（ROS）通路在慢性间歇性低氧（CIH）大鼠的升压作用。方法 将雄性SD大鼠随机分为对照组和慢性间歇性低氧组（CIH组）（8h/d,连续15d）。用立体定位仪进行PVN核团定位微量注射,采用颈动脉插管法在体测量大鼠平均动脉压（MAP）,ELISA法测量PVN中AngⅡ、ROS含量,Western blot法测定PVN中血管紧张素Ⅱ1型受体（AT1R）的蛋白表达,应用试剂盒（羟胺法）测定PVN中的总超氧化物歧化酶（T-SOD）活力。结果 与对照组比较,CIH组大鼠PVN中ROS（P〈0.05）和AngⅡ含量显著升高（P〈0.01）,AT1R的表达显著增加（P〈0.05）,而T-SOD活力则明显下降（P〈0.01）。双侧PVN内微量注射AngⅡ（0.3nmol）可升高两组大鼠的MAP,而CIH大鼠MAP升高更显著（P〈0.01）;超氧阴离子清除剂Tempol可降低两组大鼠的MAP,而CIH大鼠MAP降低更显著（P〈0.01）;Tempol预处理可抑制AngⅡ对两组大鼠的升压作用,且在CIH组中抑制作用更加明显（P〈0.01）。结论 室旁核中ROS介导了AngⅡ在CIH大鼠中的升压作用。

英文摘要：

Objective To investigate the effect of Ang II-ROS signal pathway in the hypothalamic paraventricular nucleus （PVN） on chronic intermittent hypoxia（CIH） induced-hypertension in rats. Methods Male SD rats were randomly divided into control and CIH groups. The control rats were exposed to continuous normoxia, while the CIH rats were submitted to CIH （8 h per day for 15 days）. Rats were fixed on the stereotaxic instrument to conduct microinjection in the PVN according to Paxinos and Watson rat atlas. Mean arterial pressure （MAP） was recorded in vivo on a PowerLab data acquisition system. We used ELISA kit to measure the content of Ang II , ROS, total- superoxide dismutase （T-SOD） and Western blot to measure Ang II type 1 receptor （ATIR） protein expression in PVN. Results The contents of PVN ROS （P 〈 0.05 ） and Ang II （P 〈 0. 01 ） were significantly higher than that in control rats, along with increased AT1R protein expression（P 〈 0. 05 ）. The activity of PVN T-SOD in CIH rats was significantly lower than that in control rats（P 〈0.01）. Microinjection of Ang II （0.3 nmol） in bilateral PVN in- creased MAP in both CIH and control rats, and this response was significantly augmented in CIH rats（P 〈0. 01 ）. ROS scavenger Tempol caused significant MAP decreases in CIH rats than that in control group（P 〈0. 01 ）. Tem- pol prevented Ang II-induced increases in MAP in both CIH and control rats, and this response was significantly augmented in CIH rats （P 〈 0.01 ）. Conclusion The results suggest that the ROS in PVN mediates the increased blood pressure induced by Ang II in CIH induced-hypertension rats.