The arterial baroreflex pathway provides the fundamental basis for the short term control of blood pressure via the rapid regulation of the mean level of sympathetic nerve activity (SNA) in response to changes in blood pressure. A central tenet in the generation and regulation of bursts of SNA, is that input from the arterial baroreceptors also regulates the timing of the bursts of sympathetic activity. Using an implantable telemetry based amplifier renal SNA was recorded in intact and arterial baroreceptor denervated (SAD) conscious rabbits. Data was collected continuously whilst animals were in their home cage. Mean levels of SNA were not different between SAD and baroreceptor intact animals. While SNA was unresponsive to changes in blood pressure in SAD rabbits the timing of the bursts of SNA relative to the arterial pulse wave was maintained (time between the diastolic pressure and the next maximum SNA voltage averaged 107±12 SAD vs. 105±7 ms intact). Transfer function analysis between blood pressure and SNA indicates the average gain at the heart rate frequency was not altered by SAD indicating strong coupling between the cardiac cycle and SNA bursts in SAD animals. Further experiments in anesthetized rabbits showed that this entrainment is lost immediately after performing baroreceptor denervation surgery, and remained absent while the animal was under anaesthesia, but returned within 20 min of turning off the anaesthesia. We propose this finding indicates that the regulation of the mean level of SNA requires the majority of input from baroreceptors to be functional, however the regulation of the timing of the bursts in the conscious animal requires only minimal input (like a sensitive trigger mechanism). This observation has important implications for understanding the origin and regulation of SNA.