Neurogenic Background for Emotional Stress-Associated Hypertension.
Neurogenic Background for Emotional Stress-Associated Hypertension.
复制标题
情绪应激相关高血压的神经源性背景。
DOI：
10.1007/s11906-023-01235-7
复制
发表时间：
2023-07
影响因子：
5.6
通讯作者：
中科院分区：
文献类型：
--
作者：
对自然应激源的反应涉及心脏刺激和血管变化，主要由交感神经活动的增加触发。这些影响导致立即的流量重新分配，为优先目标器官提供代谢支持，并结合其他关键生理反应和认知策略，以应对压力源挑战。这种经过数百万年进化而发展起来的极其精心策划的反应，目前正在短时间内受到挑战。在这篇简短的综述中，我们讨论了情绪应激性高血压起源的神经原性背景，重点是人类和动物的相关发现的交感神经通路。城市环境提供了各种心理压力源。真实的或预期的情绪压力源可能会增加基线交感神经活动。从日常的交通压力到与工作有关的焦虑，由情绪压力源引起的交感神经活动的慢性或异常增加可能导致心血管事件，包括心律失常，血压升高甚至猝死。在提出的各种改变中，慢性应激可以改变神经胶质细胞回路或损害抗氧化系统，从而改变神经元对应激刺激的反应。这些现象导致交感神经活动增加、高血压和随之而来的心血管疾病。焦虑、情绪压力和高血压之间的联系可能是由于控制交感神经活动的中枢通路中神经元放电率的改变。神经胶质细胞和氧化机制参与改变神经元功能主要涉及增强交感神经流出。岛皮质-背内侧下丘脑通路的增强整体交感神经流出的演变的意义进行了讨论。
The response to natural stressors involves both cardiac stimulation and vascular changes, primarily triggered by increases in sympathetic activity. These effects lead to immediate flow redistribution that provides metabolic support to priority target organs combined with other key physiological responses and cognitive strategies, against stressor challenges. This extremely well-orchestrated response that was developed over millions of years of evolution is presently being challenged, over a short period of time. In this short review, we discuss the neurogenic background for the origin of emotional stress-induced hypertension, focusing on sympathetic pathways from related findings in humans and animals. The urban environment offers a variety of psychological stressors. Real or anticipatory, emotional stressors may increase baseline sympathetic activity. From routine day-to-day traffic stress to job-related anxiety, chronic or abnormal increases in sympathetic activity caused by emotional stressors can lead to cardiovascular events, including cardiac arrhythmias, increases in blood pressure and even sudden death. Among the various alterations proposed, chronic stress could modify neuroglial circuits or compromise antioxidant systems that may alter the responsiveness of neurons to stressful stimuli. These phenomena lead to increases in sympathetic activity, hypertension and consequent cardiovascular diseases. The link between anxiety, emotional stress, and hypertension may result from an altered neuronal firing rate in central pathways controlling sympathetic activity. The participation of neuroglial and oxidative mechanisms in altered neuronal function is primarily involved in enhanced sympathetic outflow. The significance of the insular cortex-dorsomedial hypothalamic pathway in the evolution of enhanced overall sympathetic outflow is discussed.
登录
查看更多内容
影响因子：
--
作者：
Henderson, Luke A;Macefield, Vaughan G
通讯作者：
Macefield, Vaughan G
影响因子：
3.7
作者：
Grimsrud A;Stein DJ;Seedat S;Williams D;Myer L
通讯作者：
Myer L
影响因子：
2.9
作者：
Gomes da Silva, Ana Quenia;Xavier, Carlos Henrique;Fontes, Marco Antonio P.
通讯作者：
Fontes, Marco Antonio P.
影响因子：
2.5
作者：
Che, Yi;Zhou, Zhu;Wang, Jun-Feng
通讯作者：
Wang, Jun-Feng
影响因子：
2.8
作者：
Borg, Breanna A.;Rabinak, Christine A.;Marusak, Hilary A.
通讯作者：
Marusak, Hilary A.