Central control of cardiovascular function during sleep

Abstract

There is increasing evidence that cardiovascular control during sleep is relevant for cardiovascular risk. This evidence warrants increased experimental efforts to understand the physiological mechanisms of such control. This review summarizes current knowledge on autonomic features of sleep states [non-rapid-eye-movement sleep (NREMS) and rapid-eye-movement sleep (REMS)] and proposes some testable hypotheses concerning the underlying neural circuits. The physiological reduction of blood pressure (BP) during the night (BP dipping phenomenon) is mainly caused by generalized cardiovascular deactivation and baroreflex resetting during NREMS, which, in turn, are primarily a consequence of central autonomic commands. Central commands during NREMS may involve the hypothalamic ventrolateral preoptic area, central thermoregulatory and central baroreflex pathways, and command neurons in the pons and midbrain. During REMS, opposing changes in vascular resistance in different regional beds have the net effect of increasing BP compared with that of NREMS. In addition, there are transient increases in BP and baroreflex suppression associated with bursts of brain and skeletal muscle activity during REMS. These effects are also primarily a consequence of central autonomic commands, which may involve the midbrain periaqueductal gray, the sublaterodorsal and peduncular pontine nuclei, and the vestibular and raphe obscurus medullary nuclei. A key role in permitting physiological changes in BP during sleep may be played by orexin peptides released by hypothalamic neurons, which target the postulated neural pathways of central autonomic commands during NREMS and REMS. Experimental verification of these hypotheses may help reveal which central neural pathways and mechanisms are most essential for sleep-related changes in cardiovascular function.

Orexins and the cardiovascular events of awakening

“…Thereafter, both ABP and HR eventually increased approximatively 15% of their respective values during NREM sleep in wild-type mice. 36 This is in line with the observations that ABP is approximately 10% lower during NREM sleep than during wakefulness in different species, 3,4 and that changes in HR during NREM sleep may contribute to determine those of ABP by modifying cardiac output. 6,7 Inspection of Fig.…”

“…The values of ABP are approximately 10% lower during NREM sleep than during wakefulness, 3,4 which implies lower values of cardiac output and/or lower values of systemic vascular resistance (Fig. 1).…”

“…A set of testable hypotheses has been recently proposed. 4 The lower values of SNA to the skeletal muscles and kidneys during NREM sleep compared with wakefulness may result from: (a) inhibition of a "stress pathway" that involves the hypothalamic paraventricular nucleus, 21 a master autonomic and endocrine controller; 22 (b) inhibition of a "command neuron" pathway that involves the pedunculopontine nucleus of the rostral pons, 23,24 part of the mesencephalic locomotor region; 25 and (c) potentiation of a "baroreflex pathway" 26 that involves the pontine parabrachial nucleus 27 and the medullary nucleus of the solitary tract. 28 The lower values of skin SNA during NREM sleep compared with wakefulness may result from inhibition of a "thermoregulatory pathway" for heat generation and retention, which includes the hypothalamic median preoptic nucleus, the hypothalamic medial preoptic area, and the rostral medullary raphe.…”

One Neglected Yawning Function like Slow Wave Sleep: The Hypothetic Neurovascular Regulation from Mouth to Eye Driven by Expiration

“…Increases in heart rate, lung volume, and eye muscle tension have been reported during or immediately following yawning [37]. SWS manifests decrease in blood pressure [38] and complex regulation of heart rate [39]. In electrophysiology, it has been demonstrated that the sleep-wake state can modulate the inspiratory motoneurons of respiration, while the tonic expiratory units are largely unaffected by the sleep-wake state [40].…”

Distinct association between the antagonistic jaw muscle activity levels and cardiac activity during chewing and NREM sleep in the freely moving guinea pigs

“…Several studies have proposed that the correlation between motor activity level and cardiac activities (e.g., heart rate) are associated with closed-loop regulation of sympathetic nervous system during wakefulness as well as NREM sleep although two states are characterized by the different cardiac activity and sympathetic tone [6,7]. Interestingly, however, a study pointed out the possibility that the sympathetic regulation during eating behavior does not fit the cardiac-motor relationships typically seen during NREM sleep, quiet wakefulness, and waking behaviors [6].…”