Mathematical modelling provides proof of principle that phasic cardiovascular events in sleep result from integration of the arterial baroreflex and central autonomic commands

Phasic hypertensive events during sleep (PHES) occur in animal models and human subjects. PHES are accompanied by heterogeneous neurophysiological phenomena but entail a similar pattern of changes in heart rate (HR). During PHES, HR starts to increase together with blood pressure (BP), and the peak increase in HR precedes the BP peak. HR then decreases towards or below baseline while BP is still elevated. We tested in silico the hypothesis (Silvani, Clin. Exp. Pharmacol. Physiol. 2008; 35: 987-94) that changes in HR during PHES result from the integration of the baroreflex with central autonomic commands. The study was based on a mathematical model with physiological parameter values, which includes the pulsating heart, pulmonary and systemic circulations, and the arterial baroreflex (Ursino and Magosso, Am. J. Physiol. 2000; 279: H149-65). Central commands were simulated as a phasic decrease in vagal efferent activity and a simultaneous increase in sympathetic efferent activity to the heart and blood vessels. We found that the mathematical model reproduced the biphasic changes in HR that characterize PHES. This finding was robust to changes in the waveform (square vs. triangular pulse), duration, and amplitude of central commands. This result provides proof of principle that during PHES, an early increase in HR and a late decrease in HR below baseline may result from monophasic central commands because of the delays and time constants of the arterial baroreflex control.