Physiological Sleep‐dependent Changes in Arterial Blood Pressure: Central Autonomic Commands and Baroreflex Control

Abstract

SUMMARY1. Sleep is a heterogeneous behaviour. As a first approximation, it is subdivided objectively into two states: non-rapid eye movement sleep (NREMS) and rapid eye movement sleep (REMS).2. The mean value and variability of arterial blood pressure (ABP) decrease physiologically from wakefulness to NREMS. In REMS, there may be a further decrease or increase in mean ABP as well as phasic hypertensive events, which enhance the variability of ABP.3. The reduced mean ABP during NREMS results from a decrease in either heart rate or sympathetic vasoconstrictor tone. During REMS, sympathetic activity to the different cardiovascular effectors undergoes a substantial repatterning. Thus, the mean ABP in REMS reflects a balance between changes in cardiac output and constriction or dilatation of different vascular beds.4. In both sleep states, the phasic changes in ABP are driven by bursts of vasoconstriction, which may be accompanied by surges of heart rate.5. The available evidence supports the hypothesis that the sleep-dependent changes in ABP, either tonic or phasic, result from the integration between cardiovascular reflexes and central autonomic commands that are specific to each sleep state.

Sleep Modulates Hypertension in Leptin-Deficient Obese Mice

“…37 Thus, both the nature of the link between obesity and sleep and its invariance among species remain unclear. On the other hand, sleep-dependent cardiovascular changes including the decrease in BP 21,23,27,38 and the increased role of the baroreflex in cardiac control 38 -40 during NREMS are highly conserved across species, supporting the potential for extrapolation of our results. In this respect, our finding that obesity, per se (ie, in the absence of leptin), entailed increases in mean BP, which were prominent during the light (rest) period and also occurred during NREMS, may be of particular relevance.…”

“…During REMS, central autonomic commands induce vasoconstriction in the skeletal muscles 23 and vasodilatation of the mesenteric and renal vascular beds, 26 the effect of these changes on BP being buffered by sino-aortic reflexes. 27 The complexity of these factors generates the potential for interaction effects, whereby differences in BP on passing from NREMS to REMS reflect genetic 22 and possibly also pathological derangements in cardiovascular regulation.…”

“…25 On the other hand, rapid-eye-movement sleep (REMS) entails a dramatic repatterning of sympathetic activity 26 and variable changes in cardiac output. 27 On passing from NREMS to REMS, an increase in BP occurs in human subjects, 23 whereas either increases or decreases in BP are observed in different inbred mouse strains. 22 These considerations suggest that the cardiovascular effects of the wake-sleep states are a neglected yet potentially relevant source of variability in the derangements of BP, which are associated with obesity in the absence of leptin signaling.…”

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).…”