Oyarce María P, Iturriaga Rodrigo
Laboratorio de Neurobiología, Facultad de Ciencias Biológicas, Pontificia Universidad Católica de Chile, Santiago, Chile.
Front Physiol. 2018 Jul 11;9:893. doi: 10.3389/fphys.2018.00893. eCollection 2018.
Chronic intermittent hypoxia (CIH), the hallmark of obstructive sleep apnea, is the main risk factor to develop systemic hypertension. Oxidative stress, inflammation, and sympathetic overflow have been proposed as possible mechanisms underlying the CIH-induced hypertension. CIH potentiates the carotid body (CB) chemosensory discharge leading to sympathetic overflow, autonomic dysfunction, and hypertension. Oxidative stress and pro-inflammatory molecules are involved in neurogenic models of hypertension, acting on brainstem and hypothalamic nuclei related to the cardiorespiratory control, such as the nucleus of the solitary tract, which is the primary site for the afferent inputs from the CB. Oxidative stress and pro-inflammatory molecules contribute to the activation of the CB chemoreflex pathway in CIH-induced hypertension. In this brief review, we will discuss new evidence for a critical role of oxidative stress and neuro-inflammation in development of the CIH-induced hypertension through activation of the CB chemoreflex pathway.
慢性间歇性缺氧（CIH）是阻塞性睡眠呼吸暂停的标志，是引发系统性高血压的主要危险因素。氧化应激、炎症和交感神经过度兴奋被认为是CIH诱发高血压的潜在机制。CIH增强颈动脉体（CB）化学感受性放电，导致交感神经过度兴奋、自主神经功能障碍和高血压。氧化应激和促炎分子参与高血压的神经源性模型，作用于与心肺控制相关的脑干和下丘脑核团，如孤束核，它是来自CB传入输入的主要部位。氧化应激和促炎分子有助于CIH诱发高血压中CB化学感受反射通路的激活。在这篇简短的综述中，我们将讨论氧化应激和神经炎症通过激活CB化学感受反射通路在CIH诱发高血压发展中起关键作用的新证据。
