The Journal of Neurophysiology Vol. 84 No. 3 September 2000, pp. 1157-1167
Copyright ©2000 by the American Physiological Society

Modes of Baroreceptor-Sympathetic Coordination

Department of Pharmacology and Toxicology, Michigan State University, East Lansing, Michigan 48824-1317

Lewis, Craig D., Gerard L. Gebber, Sheng Zhong, Peter D. Larsen, and Susan M. Barman. Modes of Baroreceptor-Sympathetic Coordination. J. Neurophysiol. 84: 1157-1167, 2000. We tested the hypothesis that the cardiac-related rhythm in sympathetic nerve discharge (SND) results from the forcing of a central oscillator to the frequency of the heart beat by pulse-synchronous baroreceptor afferent nerve activity. For this purpose, time series analysis was used to examine the phase relations between the brachial arterial pulse (AP) and cardiac-related activity recorded from the postganglionic inferior cardiac sympathetic nerve (CN) in urethan-anesthetized cats. Specifically, we made cycle-by-cycle measurements of peak systolic blood pressure, heart period, CN burst amplitude, and the phase angle (and corresponding interval) between peak systole and the next peak of CN activity. As the steady-state level of systolic blood pressure was raised by increasing the rate of a constant intravenous infusion of phenylephrine, we observed transitions from no phase-locking of CN activity to the AP to either phase-locking of variable strength or phase walk through part of the cardiac-cycle on the time scale of respiration. Phase walk is defined as a progressive and systematic change in the phase lag of cardiac-related CN activity relative to peak systole. Raising blood pressure strengthened phase-locking and either increased or decreased the mean interval between peak systole and the next peak of CN activity even when the change in heart period was small. CN burst amplitude and the interval between peak systole and the next peak of CN activity were inversely related, but the strength of the relationship varied considerably with experimental conditions. The relationship was strongest during phase walk. Step-wise increases in blood pressure induced by abdominal aortic obstruction led to an abrupt increase in the phase lag of CN activity relative to peak systole even when heart rate was not changed. We refer to such changes as sharp phase transitions that are a general property of dynamical nonlinear systems. The results support the view that the cardiac-related rhythm in SND is a forced nonlinear oscillation rather than the consequence of periodic inhibition of randomly generated activity.