Mechanism of sympathetic activation and blood pressure elevation in humans and animals following acute intermittent hypoxia.

Sleep apnea is associated with repeated episodes of hypoxemia, causing marked increase in sympathetic nerve activity and blood pressure. Considerable evidence suggests that intermittent hypoxia (IH) resulting from apnea is the primary stimulus for sympathetic overactivity in sleep apnea patients. Several IH protocols have been developed either in animals or in humans to investigate mechanisms underlying the altered autonomic regulation of the circulation. Most of these protocols involve several days (10-40 days) of IH exposure, that is, chronic intermittent hypoxia (CIH). Recent data suggest that a single session of IH exposure, that is, acute intermittent hypoxia (AIH), is already capable of increasing tonic sympathetic nerve output (sympathetic long-term facilitation, LTF) and altering chemo- and baroreflexes with or without elevation of blood pressure. This indicates that IH alters the autonomic neurocirculatory at a very early time point, although the mechanisms underlying this neuroplasticity have not been explored in detail. The purpose of this chapter is to briefly review the effects of AIH on sympathetic LTF and alteration of autonomic reflexes in comparison with the studies from CIH studies. We will also discuss the potential central and peripheral mechanism underlying sympathetic LTF.