The arterial baroreceptors detect changes in blood pressure and form the afferent limb of the baroreflex which acts to buffer changes in pressure through reciprocal regulation of the sympathetic and parasympathetic outflow. We have previously shown that the sympathetic and parasympathetic limbs of the baroreflex operate over different pressure ranges and hypothesised that these differences in regulation of heart rate and sympathetic activity could originate from the baroafferents. We tested this hypothesis using sequential baroafferent denervations in the decerebrate, arterially perfused rat preparation. We found that baroreflex control of heart rate is critically dependent upon the aortic arch afferents with relatively little contribution from the carotid sinuses. Indeed the baroreflex bradycardia was attenuated by 85% (n=7) when only one aortic depressor nerve was cut indicating a strongly synergistic interaction between aortic baroafferents. By contrast baroreflex sympathoinhibition was dependent on inputs from all four sites, and the stimulation of any single site could elicit robust sympathoinhibition. These findings were independent of the sequence of baroafferent nerve resection (n=15). Perfusion of the isolated carotid sinus (n=5) showed that it was possible to elicit baroreflex sympathoinhibition (and changes in vascular resistance) without any significant change in heart rate despite the use of strong stimuli (>100 mmHg) or repeated pulsatile stimuli. These results indicate fundamental differences in the responses elicited by stimulation of the afferents from the carotid and aortic barosensor sites and suggest that their actions within the nucleus of the solitary tract are functionally specified (sympathetic versus parasympathetic).