Salgado HC, Barale AR, Castania JA, Machado BH, Chapleau MW, Fazan R, Jr. Baroreflex responses to electrical stimulation of aortic depressor nerve in conscious SHR. 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

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... l rats (NCR). The protocol was repeated after ␤-adrenergic-receptor blockade with atenolol. SHR exhibited higher basal MAP (150 Ϯ 5 vs. 103 Ϯ 2 mmHg) and HR (393 Ϯ 9 vs. 360 Ϯ 5 beats/min). The frequency-dependent hypotensive response to ADN stimulation was preserved or enhanced in SHR. The greater absolute fall in MAP at higher frequencies (Ϫ68 Ϯ 5 vs. Ϫ38 Ϯ 3 mmHg at 90-Hz stimulation) in SHR was associated with a preferential decrease in hindquarter (Ϫ43 Ϯ 5%) vs. mesenteric (Ϫ27 Ϯ 3%) resistance. In contrast, ADN stimulation decreased hindquarter and mesenteric resistances equivalently in NCR (Ϫ33 Ϯ 7% and Ϫ30 Ϯ 7%). Reflex bradycardia was also preserved in SHR, although its mechanism differed. Atenolol attenuated the bradycardia in SHR (Ϫ88 Ϯ 14 vs. Ϫ129 Ϯ 18 beats/min at 90-Hz stimulation) but did not alter the bradycardia in NCR (Ϫ116 Ϯ 16 vs. Ϫ133 Ϯ 13 beats/min). 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 and 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. spontaneously hypertensive rats; arterial pressure; heart rate; atenolol BARORECEPTOR AFFERENT SENSITIVITY (1, 2, 19, 43) and baroreflex-mediated changes in heart rate (HR) (25, 38) are consistently impaired in spontaneously hypertensive rats (SHR). More controversial is baroreflex control of sympathetic nerve activity, which has been reported to be impaired (8, 10), preserved (22, 33, 46) , or augmented (46) in SHR. The inconsistent findings may reflect, in part, differential baroreflex control of sympathetic activity to different regions and use of anesthesia in many of the studies. In the majority of studies, baroreflex responses were measured in response to drug-in-