Introduction

Obstructive sleep apnea (OSA) is a highly prevalent sleep disorder, characterized by repeated disruptions of breathing during sleep. The sleep fragmentation and the accompanying hypoxemia lead to many negative consequences including cardiovascular diseases, cognitive impairment, daytime sleepiness, fatigue, and depressive symptoms (Parish and Somers 2004; Reimer and Flemons 2003). Originally viewed as an interesting but rare malady, OSA is now recognized as a common disorder that is associated with major morbidity and mortality (Newman et al. 2001).

Noradrenergic activation, as indicated by augmented sympathetic neural activity, elevated circulating norepinephrine (NE) levels, and elevated urinary NE excretion, is a hallmark of OSA (Carlson, Hedner, Elam, Ejnell, Sellgren, and Wallin 1993; Dimsdale, Coy, Ziegler, Ancoli-Israel, and Clausen 1995; Fletcher 2003; Eisensehr et al. 1998).

There are numerous physiologically relevant consequences of this noradrenergic activation, including adrenergic receptor desensitization (Grote, Hraiczi, and Hedner 2000; Mills, Dimsdale, Coy, Ancoli-Israel, Clausen, and Nelesen 1995; Mills, Dimsdale, Ancoli-Israel, Clausen, and Loredo 1998; Nelesen, Dimsdale, Mills, Clausen, and Ancoli-Israel 1996), high blood pressure (Norman et al. 2006; Robinson, Stradling, and Davies 2004), and elevations in proinflammatory cytokine levels (Vgontzas et al. 2000; Yokoe et al. 2003).

This chapter will review studies that our group and others have conducted documenting neuroimmune effects of OSA, as well as studies documenting the effects of successful treatment of OSA on these physiological systems.

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