慢性间歇性低血压缺氧 降低了自发高血压大鼠的低谷底N-甲基-d-酸盐受体活性和交感外流
Xinqi Guo1, Hongyu Ma1, Ziye Cui1
1Department of Physiology, Hebei Medical University, Shijiazhuang, China.
High altitude medicine & biology
|January 19, 2024
概括
慢性间歇性低血压缺氧 (CIHH) 降低高血压大鼠的血压,通过降低下丘脑N-Methyl-d-Aspartate受体活性和交感外流. 这种效应通过改变大脑下丘脑中的氨酸 - 血管素系统来调节.
科学领域:
- 生理学 生理学 生理学
- 心血管研究研究心血管研究
- 神经科学是一个神经科学.
背景情况:
- 高血压是一个主要的心血管风险因素.
- 下丘脑内-血管酶系统 (RAS) 在血压调节中发挥作用.
- 慢性间歇性低血压缺氧 (CIHH) 已经显示出潜在的抗高血压作用.
研究的目的:
- 为了研究下丘脑RAS在CIHH的抗高血压作用中的作用.
- 确定CIHH对下丘脑N-Methyl-d-Aspartate受体 (NMDAR) 活性和自发高血压大鼠 (SHRs) 的同情性外流的影响.
主要方法:
- 在35天的时间里,SHR和Wistar-Kyoto老鼠被暴露在CIHH (模拟每天5小时的4000米高度) 中.
- 测量包括血压,RAS成分 (血管新生素II,Ang1-7) 和NMDAR活动在下丘脑侧腔核 (PVN),以及交感神经活动.
- 药理干预 (A779, ангиотензин II, Ang 1-7) 用于阐明机制.
主要成果:
- 在SHRs中,CIHH显著降低了缩,腹缩和平均动脉血压,治疗后的持续效果.
- 在SHR中,CIHH逆转了下丘脑ACE/AngII/AT1和ACE2/Ang1-7/Mas轴的变化.
- CIHH降低了SHRs的PVN前交感神经元中的前和后交感NMDAR活性,这种效应被Ang1-7模仿并被A779或AngII阻止.
结论:
- CIHH通过调节下丘脑RAS活性,对SHRs产生抗高血压作用.
- 通过降低ACE/AngII/AT1轴活动和增加ACE2/Ang1-7/Mas轴活动,CIHH降低了交感外流和血压.
- CIHH的抗高血压作用包括减少PVN前交感神经元中的NMDAR活性.
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