Affiliation:
1. Laboratorio de Neurobiología, Facultad de Ciencias Biológicas Pontificia Universidad Católica de Chile Santiago Chile
2. Centro de Investigación en Fisiología y Medicina de Altura, Facultad de Ciencias de la Salud Universidad de Antofagasta Antofagasta Chile
Abstract
AbstractObstructive sleep apnoea (OSA), characterized by chronic intermittent hypoxia (CIH), is considered to be an independent risk for hypertension. The pathological cardiorespiratory consequences of OSA have been attributed to systemic oxidative stress, inflammation and sympathetic overflow induced by CIH, but an emerging body of evidence indicates that a nitro‐oxidative and pro‐inflammatory milieu within the carotid body (CB) is involved in the potentiation of CB chemosensory responses to hypoxia, which contribute to enhance the sympathetic activity. Accordingly, autonomic and cardiovascular alterations induced by CIH are critically dependent on an abnormally heightened CB chemosensory input to the nucleus of tractus solitarius (NTS), where second‐order neurons project onto the rostral ventrolateral medulla (RVLM), activating pre‐sympathetic neurons that control pre‐ganglionic sympathetic neurons. CIH produces oxidative stress and neuroinflammation in the NTS and RVLM, which may contribute to the long‐term irreversibility of the CIH‐induced alterations. This brief review is mainly focused on the contribution of nitro‐oxidative stress and pro‐inflammatory molecules on the hyperactivation of the hypoxic chemoreflex pathway including the CB and the brainstem centres, and whether the persistence of autonomic and cardiorespiratory alterations may depend on the glial‐related neuroinflammation induced by the enhanced CB chemosensory afferent input.
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Funder
Fondo Nacional de Desarrollo Científico y Tecnológico
Cited by
5 articles.
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