Oxidative Stress in the Carotid Body: Implications for the Cardioventilatory Alterations Induced by Obstructive Sleep Apnea

Contribution of Autonomic Nervous System to the Hypertension Induced by Obstructive Sleep Apnea

“…Thus, the available data support the idea that the enhanced chemoreflex response observed in OSA patients is produced by the intermittent hypoxia. Similarly, animals exposed to chronic intermittent hypoxia show enhanced hypoxic ventilatory responses to acute hypoxia [15,18,43,44,87] and long-term facilitation of respiratory motor responses [63,83,88]. Recording of chemosensory nerve impulses from the carotid sinus nerve have confirmed the idea that chronic intermittent hypoxia produces long-term facilitation of the carotid body chemosensory responses to hypoxia.…”

“…These results agree and extend previous observations that antioxidant pretreatment prevented the carotid body chemosensory potentiation [80,82] and the hypertension [106] in rats exposed to intermittent hypoxia. Although, these results strongly suggest that the carotid body chemosensory potentiation is mediated by oxidative stress [15,43,44,80], it is matter of debate if ROS perse increases the carotid body chemosensory discharges [32]. Thus, it is likely that other molecule downstream the ROS signals mediate the effects of ROS on carotid body chemoreception induced by intermittent hypoxia.…”

“…During the airflow occlusion, the resulting hypoxia and hypercapnia stimulates the carotid body chemoreceptors producing reflex ventilatory, sympathetic and hypertensive responses. Among these disturbances, the chronic intermittent hypoxia is considered the main factor for the development of the hypertension [1,19,33,41,43,51,55,56,82,83,88,93,100]. However, conclusions from studies performed in OSA patients are partial and somehow controversial, because invasive procedures are precluded because of ethical reasons in humans, and OSA patients often present concomitant morbidities (i.e.…”

“…26] found that the bilateral carotid body denervation prevented the hypertension in rats exposed to chronic intermittent hypoxia, suggesting that the carotid body contributes to the cardiovascular pathologies induced by OSA. In the last years, the proposal that the carotid body is involved in the progression of the intermittent hypoxiainduced hypertension received substantial attention [19,22,25,28,41,43,98,100].…”

“…The most accepted explanation proposes that chronic intermittent hypoxia produces oxidative stress, inflammation, and sympathetic hyperactivity, which led to endothelial dysfunction and hypertension [19,25,28,41,43,52,53,65,99,100], but it is likely that intrathoracic pressure changes causing excessive mechanical stress on large artery walls and the heart, and arousal-induced sympathetic hyperactivity may also contribute to the endothelial dysfunction [47]. OSA is characterized by repeated episodes of total or partial airflow detention during sleep produced by the pharyngeal collapse, eliciting intermittent hypoxia and hypercapnia, negative intrathoraxic pressure, sleep fragmentation and arousal.…”