-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 ␤-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-induced changes in arterial blood pressure (BP), which does not allow assessment of reflex changes in vascular resistance.The goal of the present study was to compare the magnitude of reflex responses to electrical stimulation of baroreceptor afferents in the aortic depressor nerve (ADN) in conscious normotensive control rats (NCR) and SHR. This approach allowed us to assess not only the fall in HR but also the decrease in BP and regional vascular resistances. Furthermore, we hypothesized that electrical activation of baroreceptor afferents would more eff...

The time to reach the maximum response of arterial pressure, heart rate and vascular resistance (hindquarter and mesenteric) was measured in conscious male spontaneously hypertensive (SHR) and normotensive control rats (NCR; Wistar; 18-22 weeks) subjected to electrical stimulation of the aortic depressor nerve (ADN). The parameters of stimulation were 1 mA intensity and 2 ms pulse length applied for 5 s, using frequencies of 10, 30, and 90 Hz. The time to reach the hemodynamic responses at different frequencies of ADN stimulation was similar for SHR (N = 15) and NCR (N = 14); hypotension = NCR (4194 ± 336 to 3695 ± 463 ms) vs SHR (3475 ± 354 to 4494 ± 300 ms); bradycardia = NCR (1618 ± 152 to 1358 ± 185 ms) vs SHR (1911 ± 323 to 1852 ± 431 ms), and the fall in hindquarter vascular resistance = NCR (6054 ± 486 to 6550 ± 847 ms) vs SHR (4849 ± 918 to 4926 ± 646 ms); mesenteric = NCR (5574 ± 790 to 5752 ± 539 ms) vs SHR (5638 ± 648 to 6777 ± 624 ms). In addition, ADN stimulation produced baroreflex responses characterized by a faster cardiac effect followed by a vascular effect, which together contributed to the decrease in arterial pressure. Therefore, the results indicate that there is no alteration in the conduction of the electrical impulse after the site of baroreceptor mechanical transduction in the baroreflex pathway (central and/or efferent) in conscious SHR compared to NCR.