Bidirectional interactions between the baroreceptor reflex and arousal: an update

Cardiovascular autonomic dysfunctions and sleep disorders

“…The arterial baroreceptors are mechanoreceptors M A N U S C R I P T A C C E P T E D ACCEPTED MANUSCRIPT 8 mainly located in the carotid sinuses and aortic arch, innervated by the glossopharyngeal and vagus nerves, which respond to changes in carotid or aortic stretch elicited by rises or falls in arterial BP and provide inputs to the nucleus of the solitary tract (NTS) (Figure 1) [5]. Baroreflex activity is modulated by areas of the central autonomic network like the hypothalamus whose top-down inputs directed to the NTS contribute to short-and long-term BP control [5][6][7]. However, the NTS also has a bottom-up modulatory role exerted by its ascending projections to the upper brain.…”

“…However, the NTS also has a bottom-up modulatory role exerted by its ascending projections to the upper brain. This reciprocal interaction suggests that changes in baroreflex afferent activity may influence the higher level of autonomic control, including the mechanisms adjusting the sleep-wake cycle [5][6][7].…”

“…Further changes in EEG activity, with the appearance of EEG signs of cortical or subcortical arousal (intermittent alpha rhythm, K-complex sequences, and slow wave sequences), associated with increases in BP, HR, and ventilation occur periodically every 20 to 30 seconds during NREM sleep [23,24] or transiently as part of the physiological response to an arousing stimulus [7,25].…”

Orexins and the cardiovascular events of awakening

“…89 The increase in ABP upon awakening may be part of a positive feedback control that prevents uncontrolled transitions back to sleep Phasic increases in ABP may promote awakening from NREM sleep. 90 In particular, 10-20 mmHg increases in ABP obtained with pharmacological 91,92 or mechanical 91,93 means increased the probability of arousal from NREM sleep in experiments on dogs, 91 lambs, 93 and human subjects. 92 At least in lambs, this phenomenon was neither an experimental artifact nor a byproduct of changes in brain circulation, because it was prevented by sectioning baroreceptor afferents.…”

“…88 These considerations suggest that efferent connections from the nucleus of the solitary tract to the parabrachial nucleus may promote awakening in response to increases in ABP. 90 The activity of parabrachial nucleus neurons is generally lower during NREM sleep than during wakefulness, 27,98 potentially because of inhibition by the hypothalamic ventrolateral preoptic nucleus 30 and, possibly, also by local neurons. 99 Increases in parabrachial nucleus activity may inhibit the baroreflex.…”