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1Department of Physiology, School of Medicine of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil; and 2Departments of Internal Medicine and Physiology and Biophysics, University of Iowa and Veterans Affairs Medical Center, Iowa City, Iowa
Submitted 20 February 2006 ; accepted in final form 31 August 2006
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 (590 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 ± 5 vs. 103 ± 2 mmHg) and HR (393 ± 9 vs. 360 ± 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 (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 beats/min at 90-Hz stimulation) but did not alter the bradycardia in NCR (116 ± 16 vs. 133 ± 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
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