In intact animals the circulatory responses evoked by transmitter released from specific neurons of the central nervous system (CNS), or by centrally administered drugs, depend on the direct effects initiated in the CNS plus secondary reflex changes in autonomic activity. We have studied the contribution of the arterial baroreceptor reflexes to the mean arterial pressure (MAP) and heart rate responses produced by intracisternal (i.c.) clonidine and during the first few hours after i.c. 6-hydroxydopamine (6-OHDA), which releases transmitter from noradrenergic neurons. The direct and reflex components were assessed from the differences in responses between intact and sino-aortic denervated (SAD) rabbits, with the latter's responses taken to approximate the direct CNS-induced effects. The direct effects of transmitter release were (a) an early fall in MAP followed by a late pressor effect; and (b) an early bradycardia followed by a late tachycardia. The early responses were similar to the direct effects of i.c. clonidine and to the findings observed in pontine rabbits with intact baroreceptors. In intact rabbits, feedback through the arterial baroreceptors reduced the fall in MAP with clonidine, but had no effect on the heart rate changes. Similarly, it eliminated the early depressor response to 6-OHDA but had little effect on the early bradycardia; however, the late pressor response was little affected, and the late tachycardia was masked by a reflex bradycardia. Our findings suggest that arterial baroreceptor reflexes can modify some effects initiated in the CNS, but some of the pathways are not involved in this interaction.