. Dynamic baroreflex control of blood pressure: influence of the heart vs. peripheral resistance. Am J Physiol Regulatory Integrative Comp Physiol 283: R533-R542, 2002; 10.1152/ajpregu.00489.2001The aim in the present experiments was to assess the dynamic baroreflex control of blood pressure, to develop an accurate mathematical model that represented this relationship, and to assess the role of dynamic changes in heart rate and stroke volume in giving rise to components of this response. Patterned electrical stimulation [pseudo-random binary sequence (PRBS)] was applied to the aortic depressor nerve (ADN) to produce changes in blood pressure under open-loop conditions in anesthetized rabbits. The stimulus provided constant power over the frequency range 0-0.5 Hz and revealed that the composite systems represented by the central nervous system, sympathetic activity, and vascular resistance responded as a second-order low-pass filter (corner frequency Ϸ0.047 Hz) with a time delay (1.01 s). The gain between ADN and mean arterial pressure was reasonably constant before the corner frequency and then decreased with increasing frequency of stimulus. Although the heart rate was altered in response to the PRBS stimuli, we found that removal of the heart's ability to contribute to blood pressure variability by vagotomy and ␤ 1-receptor blockade did not significantly alter the frequency response. We conclude that the contribution of the heart to the dynamic regulation of blood pressure is negligible in the rabbit. The consequences of this finding are examined with respect to low-frequency oscillations in blood pressure. sympathetic nerve activity; modeling; transfer function; vasculature; rabbit THE ABILITY OF THE ARTERIAL baroreflex pathway to regulate blood pressure under steady-state conditions is well understood (25). However, there is a paucity of information regarding its dynamic ability over the frequency range 0.001-0.5 Hz. This is particularly relevant when trying to understand the mechanisms that give rise to oscillations between 0.1 and 0.4 Hz. Although there is general acceptance that this oscillation seen in humans at 0.1 Hz involves an action of the sympathetic nervous system on the vasculature, it is a matter of debate as to the origin of the oscillation. It has been suggested that the oscillation results either as a by-product of the central generation of sympathetic nerve activity (SNA) (8,24) or from the time delay between the arterial baroreceptors sensing blood pressure and the subsequent reflex effect on the vasculature (3,6,9,22,29). Certainly the available evidence suggests that the oscillation requires the presence of each of the components of the baroreflex pathway, with baroreceptor denervation or sympathectomy abolishing the oscillation in blood pressure (7,16,19). Clearly, if measurement of the strength of such oscillations is to develop into a clinically useful tool, it is imperative to understand factors from which cardiovascular variability is derived (23).Although it is clear that SNA to t...