Inflammation and oxidative stress during intermittent hypoxia: the impact on chemoreception

What is the topic of this review? This article describes the contribution of oxidative stress and pro-inflammatory cytokines to the enhanced carotid body chemosensory responsiveness to the hypoxia and systemic hypertension induced by chronic intermittent hypoxia. What advances does it highlight? Chronic intermittent hypoxia enhances the carotid body chemosensory discharge during normoxia and hypoxia, leading to sympathetic overactivity and hypertension. New evidence suggests that chronic intermittent hypoxia increases pro-inflammatory cytokines. Here, we discuss the role of inflammation in the alterations of the carotid chemoreceptor function as well as the cardiorespiratory alterations following chronic intermittent hypoxia. Chronic intermittent hypoxia (CIH), the main characteristic of obstructive sleep apnoea, enhances carotid body (CB) chemosensory discharges during normoxia and hypoxia and elicits hypertension. These alterations are attributed to oxidative stress, because antioxidants prevent the enhanced CB chemosensory discharges and the hypertension. In this report, we discuss new evidence supporting the suggestion that oxidative stress-induced upregulation of pro-inflammatory cytokines (i.e. tumour necrosis factor-α and interleukin-1β) in the CB is involved in the chemosensory potentiation and the hypertension following CIH. Anti-inflammatory treatment with ibuprofen prevents the increased tumour necrosis factor-α and interleukin-1β levels in the CB and the hypertension, but does not reduce the enhanced chemosensory hypoxic response and the local oxidative stress in the CB. In contrast, antioxidant treatment with ascorbic acid prevents the increase in cytokine concentrations and CB oxidative stress, the chemosensory potentiation and the hypertension. Thus, the enhanced CB chemosensory responses to hypoxia depend critically on the oxidative stress, but not on the increased tumour necrosis factor-α and interleukin-1β in the CB. We discuss a possible role for pro-inflammatory cytokines in development of the hypertension produced by CIH, acting on cardiorespiratory centres located in the CNS.