Sleep is a natural periodic suspension of consciousness during which processes of rest and restoration occur. The cognitive, reparative and regenerative accompaniments of sleep appear to be essential for maintenance of health and homeostasis. This brief overview will examine the cardiovascular responses to normal and disordered sleep, and their physiologic and pathologic implications. In the past, sleep was believed to be a passive state. The tableau of sleep as it unfolds is anything but a passive process. The brain's activity is as complex as wakefulness, never "resting" during sleep. Following the demise of the 'passive theory of sleep' (the reticular activating system is fatigued during the waking day and hence becomes inactive), there arose the 'active theory of sleep' (sleep is due to an active general inhibition of the brain) (1). Hess demonstrated the active nature of sleep in cats, inducing "physiological sleep" with electrical stimulation of the diencephalon (2). Classical experiments of transection of the cat brainstem (3) at midpontine level inhibited sleep completely, implying that centers below this level were involved in the induction of sleep (1, 4). For the first time, measurement of sleep depth without awakening the sleeper using the electroencephalogram (EEG) was demonstrated in animals by Caton and in humans, by Berger (1). This was soon followed by discovery of the rapid eye movement sleep periods (REM) by Aserinski and Kleitman (5), demonstration of periodical sleep cycles and their association with REM sleep (6, 7). Multiple studies and steady discoveries (4) made polysomnography, with its ability to perform simultaneous whole night recordings of EEG, electromyogram (EMG), and electrooculogram (EOC), a major diagnostic tool in study of sleep disorders. This facility has been of further critical importance in allowing evaluation of the interaction between sleep and changes in hemodynamics and autonomic cardiovascular control. Consequently the effects of sleep could be objectively differentiated from the effects of rest and recumbency. Furthermore, the specific effects of sleep onset and termination, and the effects of different sleep stages, could be assessed. Technological advances, with consequently enhanced and relatively non-invasive approaches to cardiovascular regulation, have greatly broadened our understanding of the effects of sleep stage on cardiovascular function. Continuous monitoring of simultaneous measures of polysomnographic and cardiovascular variables enables characterization of the effects of dynamic changes and rapid transitions in sleep stage, such as arousals. The capacity for measuring acute and immediate changes in autonomic, EEG and hemodynamic responses to sleep and arousal on a continuous basis has played an important role in enabling us to understand the interplay between changes in EEG and changes in the more peripheral measurements of neural and circulatory variables, such as sympathetic nerve traffic, heart rate (HR) and blood pressure (BP). Measurements of heart rate variability (HRV) (8-10), baroreflex sensitivity (BRS) (11-16), and intraneural measurement of sympathetic nerve traffic to muscle (MSNA) (17-22) and skin (SSNA) (23-24) have further advanced our understanding of mechanisms linking sleep and cardiovascular physiology.