创伤后应激障碍通过PVN激活和Sprague Dawley大鼠的血管功能障碍增加高血压发展的风险.
Xinqian Chen1,2, Xin Yan2,3, Chunxiu Yu2,4
1Department of Kinesiology and Integrative Physiology, Michigan Technological University, Houghton, MI 49931, USA.
Antioxidants (Basel, Switzerland)
|November 27, 2024
概括
单一的长期压力 (SPS),创伤后应激障碍 (PTSD) 的模型,主要是心血管路径. 这种压力模型增加了氧化压力和炎症,可能导致高血压和未来的压力因素.
科学领域:
- 神经科学是一个神经科学.
- 心血管科学 心血管科学
- 压力生理学 压力生理学
背景情况:
- 创伤后应激障碍 (PTSD) 与心血管问题有关.
- 单一长期压力 (SPS) 是一种模拟PTSD的动物模型.
- 连接压力,大脑和心血管功能障碍的机制需要阐明.
研究的目的:
- 为了研究SPS对心血管反应的影响,下丘脑副心室核 (PVN) 活动和血管功能.
- 探索将创伤性压力与高血压联系起来的分子机制.
- 确定与压力有关的心血管疾病的潜在治疗点.
主要方法:
- 雄性斯普拉格·道利大鼠接受了SPS.
- 对心血管参数 (血压,心率) 进行监测.
- 在PVN和大动脉中分析了基因表达 (血压素,AT1R,FOSL1,TNFα,IL1β,iNOS).
- 评估了线粒体反应性氧物种 (mtROS) 和血管反应性.
主要成果:
- SPS诱导血压和心率的短暂增加,但不是慢性高血压.
- 在PVN中观察到高血压相关基因 (血压素,AT1R,FOSL1) 的改变表达.
- 升高的mtROS与PVN中的AT1R和FOSL1共定位,表明氧化应激放大.
- SPS增加了主动脉中的促炎性细胞因子和iNOS,损害了血管功能.
结论:
- SPS使神经内分泌,自主和血管通路敏感,造成心血管脆弱性.
- 氧化应激和改变的PVN通路是将压力与心血管功能障碍联系起来的关键机制.
- 准氧化应激和PVN通路可能会减轻PTSD对心血管的影响.
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