Baroreflex responses to changes in arterial pressure are impaired in spontaneously hypertensive rats (SHR). Mean arterial pressure (MAP), heart rate (HR), and regional vascular resistances were measured before and during electrical stimulation (5-90 Hz) of the left aortic depressor nerve (ADN) in conscious SHR and normotensive control rats (NCR). The protocol was repeated after ₁-adrenergic receptor blockade with atenolol. SHR exhibited higher basal MAP (150±5 vs. 103±2 mmHg) and HR (393±9 vs. 360±5 bpm). The frequency-dependent hypotensive response to ADN stimulation was preserved or enhanced in SHR. The greater absolute fall in MAP at higher frequencies (-68±5 vs. -38±3 mmHg at 90 Hz stimulation) in SHR was associated with a preferential decrease in hindquarter (-43±5%) vs. mesenteric (-27±3%) resistance. In contrast, ADN stimulation decreased hindquarter and mesenteric resistances equivalently in NCR (-33±7% and -30±7%). Reflex bradycardia was also preserved in SHR although its mechanism differed. Atenolol attenuated the bradycardia in SHR (-88±14 vs. -129±18 bpm at 90 Hz stimulation), but did not alter the bradycardia in NCR (-116±16 vs. -133±13 bpm). The residual bradycardia under atenolol (parasympathetic component) was reduced in SHR. MAP and HR responses to ADN stimulation were also preserved or enhanced in SHR vs. NCR after deafferentation of carotid sinuses as contralateral right ADN. The results demonstrate distinct differences in central baroreflex control in conscious SHR vs. NCR. Inhibition of cardiac sympathetic tone maintains reflex bradycardia during ADN stimulation in SHR despite impaired parasympathetic activation, and depressor responses to ADN stimulation are equivalent or even greater in SHR due to augmented hindquarter vasodilation.