TY - JOUR
T1 - Bidirectional interactions between the baroreceptor reflex and arousal
T2 - an update
AU - Silvani, Alessandro
AU - Calandra-Buonaura, Giovanna
AU - Benarroch, Eduardo E.
AU - Dampney, Roger A L
AU - Cortelli, Pietro
PY - 2015/2/1
Y1 - 2015/2/1
N2 - Studies involving genetic engineering on animal models and mathematical analysis of cardiovascular signals on humans are shedding new light on the interactions between the arterial baroreceptor reflex (baroreflex) and arousal. Baroreceptor stimulation, if very mild or performed under anaesthesia, may inhibit cortical arousal. However, substantial increases or decreases in baroreflex activation cause arousal in animal models and human subjects in physiological conditions. On the other hand, cardiovascular changes during autonomic arousals and between the states of wakefulness and sleep involve changes in the baroreflex set point and balance with central autonomic commands. Neural connectivity and functional data suggest that the nucleus of the solitary tract, adrenergic C1 neurons of the medulla, and the parabrachial nucleus of the pons mediate the bidirectional interactions between the baroreflex and arousal. These interactions may constitute a positive feedback loop that facilitates sharp and coordinated brain state and autonomic transitions upon arousal: upon arousal, central autonomic commands may increase blood pressure, thereby loading baroreceptors and further increasing arousal. Anomalies of this feedback loop may play a role in the pathophysiology of disease conditions associated with cardiovascular and sleep-wake cycle alterations. These conditions include: obstructive sleep apnoea syndrome, with its association with excessive daytime sleepiness and baroreflex impairment; and insomnia, with its association with autonomic hyperarousal and hypertension. When faced with disorders associated with cardiovascular and sleep-wake cycle alterations, clinical reasoning should entertain the possibility that both conditions are strongly influenced by anomalies of baroreflex function.
AB - Studies involving genetic engineering on animal models and mathematical analysis of cardiovascular signals on humans are shedding new light on the interactions between the arterial baroreceptor reflex (baroreflex) and arousal. Baroreceptor stimulation, if very mild or performed under anaesthesia, may inhibit cortical arousal. However, substantial increases or decreases in baroreflex activation cause arousal in animal models and human subjects in physiological conditions. On the other hand, cardiovascular changes during autonomic arousals and between the states of wakefulness and sleep involve changes in the baroreflex set point and balance with central autonomic commands. Neural connectivity and functional data suggest that the nucleus of the solitary tract, adrenergic C1 neurons of the medulla, and the parabrachial nucleus of the pons mediate the bidirectional interactions between the baroreflex and arousal. These interactions may constitute a positive feedback loop that facilitates sharp and coordinated brain state and autonomic transitions upon arousal: upon arousal, central autonomic commands may increase blood pressure, thereby loading baroreceptors and further increasing arousal. Anomalies of this feedback loop may play a role in the pathophysiology of disease conditions associated with cardiovascular and sleep-wake cycle alterations. These conditions include: obstructive sleep apnoea syndrome, with its association with excessive daytime sleepiness and baroreflex impairment; and insomnia, with its association with autonomic hyperarousal and hypertension. When faced with disorders associated with cardiovascular and sleep-wake cycle alterations, clinical reasoning should entertain the possibility that both conditions are strongly influenced by anomalies of baroreflex function.
KW - Arousal
KW - Baroreceptors
KW - Hypertension
KW - Insomnia
KW - Sleep
KW - Sleep-disordered breathing
UR - http://www.scopus.com/inward/record.url?scp=84923295109&partnerID=8YFLogxK
U2 - 10.1016/j.sleep.2014.10.011
DO - 10.1016/j.sleep.2014.10.011
M3 - Review article
C2 - 25616389
AN - SCOPUS:84923295109
SN - 1389-9457
VL - 16
SP - 210
EP - 216
JO - Sleep Medicine
JF - Sleep Medicine
IS - 2
ER -