Abstract
Sleep is involved in the regulation of major organ functions in the human body, and disruption of sleep potentially can elicit organ dysfunction. Obstructive sleep apnea (OSA) is the most prevalent sleep disorder of breathing in adults and children, and its manifestations reflect the interactions between intermittent hypoxia, intermittent hypercapnia, increased intra-thoracic pressure swings, and sleep fragmentation, as elicited by the episodic changes in upper airway resistance during sleep. The sympathetic nervous system is an important modulator of the cardiovascular, immune, endocrine and metabolic systems, and alterations in autonomic activity may lead to metabolic imbalance and organ dysfunction. Here we review how OSA and its constitutive components can lead to perturbation of the autonomic nervous system in general, and to altered regulation of catecholamines, both of which then playing an important role in some of the mechanisms underlying OSA-induced morbidities.
Highlights
Obstructive sleep apnea (OSA) is the most prevalent form of sleep disordered breathing
SUMMARY Considering the close relationships between sleep regulatory mechanisms and autonomic nerve system function described heretofore, any sleep disturbance can theoretically lead to alterations in sympathetic activity, and may elicit metabolic and cardiovascular morbidities
Conclusive evidence has become available to indicate that OSA components lead to pathological activation of the sympathetic nervous system and contribute to the pathophysiology of high blood pressure, arrhythmias, and congestive heart failure in adults
Summary
Obstructive sleep apnea (OSA) is the most prevalent form of sleep disordered breathing. Sleep state transitions are accompanied by other changes in the cardiovascular system, for example, when transitioning from NREM sleep to REM sleep, blood pressure, and heart rate typically increase and become more unstable (Schwimmer et al, 2010) These phenomena are altered in OSA patients, and are believed to underlie the increased risk for development of hypertension, one of the important cardiovascular morbidities of the disorder. When rodents were exposed to IH, attenuated baroreflex function, sensitivity and activity, or changes in the reflex set point depending on the severity of the hypoxia stimulus developed over time (Brooks et al, 1999; Greenberg et al, 1999; Lai et al, 2006; Gu et al, 2007; Peng et al, 2012) These changes led to exaggerated sympathetic activity and eventually elicited elevations of blood pressure and the elimination of the normal blood pressure dipping during sleep.
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