Controversy surrounds the respiratory responses to baroreceptor activation. Although many reflexes that effect respiration (e.g. chemoreflexes and nociceptive reflexes) frequently affect cardiovascular parameters, the effect of baroreflex stimulation within normal physiological limits is generally considered to affect only blood pressure and heart rate. Even though previous authors have reported that baroreceptor activation can affect respiratory activity, the effects on respiratory frequency and amplitude are highly variable, and changes in perfusion evoked by blood pressure manipulation could account for the observed effects. Here, we determined the respiratory effects of activating arterial baroreceptors by intravenous injection of phenylephrine or angiotensin II, or by electrical stimulation of the aortic depressor nerve (ADN). In urethane-anesthetized vagotomized rats, 1, 2 and 4 s trains of tetanic ADN stimulation evoked 3.1 ± 1.1%, 11.2 ± 13.6% and 21.9 ± 8.9% increases in inspiratory (TI) time and 26.5 ± 18%, 23.4 ± 15.7% and 34.6 ± 20.9% increases in expiratory (TE) time, respectively (P < 0.05 in both cases), but no effect on the amplitude of bursts recorded in the phrenic nerve. Similar effects were observed following pressor trials evoked by intravenous PE (TE: +26.1 ± 9.1%, P < 0.01), but not Ang II. Intermittent ADN stimulation (single pulse, 1 Hz) significantly increased the variability of TI during periods of low respiratory drive (P < 0.05) without significantly affecting any other parameters. We propose that a specific baroreceptor-respiratory response exists that is independent of changes in blood flow. In contrast to the effects of baroreceptor stimulation on sympathetic nerve activity, the baro-respiratory response is subtle and highly dependent on respiratory drive.