Inflammation, nitro‐oxidative stress and altered autonomic outflow in obstructive sleep apnoea: an assault on homeostasis

Abstract

The carotid body (CB) acts as a chemoreceptor which, when stimulated by arterial hypoxia, hypercapnia or acidosis, releases transmitters which stimulate sensory afferents that signal to the nucleus tractus solitarius (NTS). Acting through the rostral ventrolateral medulla (RVLM), this initiates a chemoreflex, stimulating autonomic efferents that orchestrate compensatory cardiorespiratory responses. Unfortunately, chronic intermittent hypoxia (CIH), which occurs in obstructive sleep apnoea (OSA), subverts the beneficial homeostatic function of this chemoreflex, causing increases in basal and hypoxia-induced transmitter release by the CB and sensitizing the cardiorespiratory centres it acts through. This causes a chronic sympathetic overdrive, contributing to the pathophysiological consequences of OSA such as heart failure, resistant hypertension and insulin resistance. [Texto del artículo]