Differential baroreflex control of heart rate and vascular resistance in rabbits. Relative role of carotid, aortic, and cardiopulmonary baroreceptors.

Guo, G. B.; Thames, Marc D.; Abboud, François M.

doi:10.1161/01.res.50.4.554

Cited by 93 publications

(59 citation statements)

References 44 publications

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“…Similar findings in the dog were reported by Ito and Scher,7 8 whose chronic denervation experiments suggested that reflex heart rate responses are impaired to a greater extent by aortic baroreflex denervation than by carotid denervation. In contrast, Guo et al 9 have shown that the CBR and ABR exert similar degrees of vagally mediated heart rate control in anesthetized rabbits during PE-induced hypertension. Furthermore, their studies suggested that there was essentially no redundancy of carotid and aortic baroreceptor afferents with regard to activation of vagal neurons, but that there was essentially "total redundancy" of these arterial baroreceptors with respect to inhibition of sympathetic efferent neurons.…”

Section: Discussionmentioning

confidence: 85%

Arterial baroreflex control of sympathetic nerve activity during elevation of blood pressure in normal man: dominance of aortic baroreflexes.

1988

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Arterial baroreceptors in the carotid sinus (CBR) and aortic arch (ABR) regions exert important control over heart rate and peripheral vascular responses to changes in arterial pressure. The relative roles of these two baroreflex pathways on control of sympathetic nerve activity during sustained elevation of arterial pressure in man is unknown. We therefore studied the relative contributions of the carotid versus the aortic baroreflexes on the control of muscle sympathetic nerve activity (MSNA) during elevation ofarterial pressure in normal human subjects. In eight normal men (group I), we measured MSNA (microneurography) during sustained elevation of arterial pressure produced by intravenous infusion of phenylephrine (PE) alone (combined ABR and CBR activation) versus during PE infusion with superimposed application of sustained external neck pressure (NP). NP was applied during sustained PE infusion to eliminate the increase in transmural carotid sinus pressure and thus remove CBR activation, thereby causing ABR stimulation alone. Mean arterial pressure was measured directly, central venous pressure was held constant during PE infusion, and MSNA was measured as total activity (burst frequency x amplitude) and expressed as units. Infusion of PE (ABR and CBR activation) increased mean arterial pressure from 87.2 + 2.8 to 94.9 ± 2.9 mm Hg (± SE, p<.001). This was accompanied by a decrease in heart rate from 65.8 ± 3.4 to 56.1 ± 3.3 beats/min (p<.001) and a decrease in MSNA from 236.2 ± 47.5 to 84.5 ± 19.3 units (p<.001). During infusion of PE with superimposed NP (ABR activation alone), mean arterial pressure increased further to 101.2 ± 2.9 mm Hg (p<.001 versus control or PE alone), and heart rate returned to control levels of 62.9 ± 2.0 beats/min (p = NS vs control; p<.01 PE vs PE plus NP), but MSNA remained reduced at 48.6 ± 9.2 units (p< .01 vs control; p = NS vs PE alone). Thus, combined activation of ABR and CBR resulted in a 65 + 5% attenution of MSNA, while activation of ABR alone resulted in a 73 ± 7% attenuation of MSNA. In a separate series of experiments in seven subjects (group II) we used sustained external neck suction alone to activate the CBR (leaving the ABR either unchanged or minimally deactivated) and studied the MSNA responses to this CBR activation.Application of -17.5 + 1.3 mm Hg of neck suction resulted in a decrease in mean arterial pressure from 83.9 ± 2.7 to 78.7 ± 3.5 mm Hg (p<.01). This was associated with a tendency for a decrease in heart rate from 62.0 ± 2.0 to 58.2 ± 2.3 beats/min (p = .05). This activation of CBR by external neck suction was not associated with a sustained decrease in MSNA (MSNA control = 188.9 ± 50.1 units vs MSNA during NS = 168.3 + 44.3 units, p = NS). These results demonstrate that the aortic baroreflexes alone produce a substantial and sustained inhibition of MSNA during elevation of arterial pressure in normal man, whereas stimulation of carotid baroreflexes alone does not produce a significant sustained inhibition of MSNA.

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Section: Discussionmentioning

confidence: 85%

Arterial baroreflex control of sympathetic nerve activity during elevation of blood pressure in normal man: dominance of aortic baroreflexes.

1988

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“…Similar findings in the dog were reported by Ito and Scher (2,3) in which chronic denervation experiments suggested that reflex heart rate responses are impaired to a greater extent by aortic baroreflex denervation than by carotid denervation. In contrast, Guo et al (4) have shown the carotid and aortic baroreceptors exert similar degrees of vagally mediated heart rate control in anesthetized rabbits during phenylephrine (PE)-induced' hypertension. Furthermore, their studies suggested that there was essentially no redundancy of carotid and aortic baroreceptor afferents with regard to activation of vagal neurons, but that there was essentially "total redundancy" of these arterial baroreceptors with respect to inhibition of sympathetic efferent neurons.…”

Section: Introductionmentioning

confidence: 92%

Relative contribution of aortic and carotid baroreflexes to heart rate control in man during steady state and dynamic increases in arterial pressure.

Ferguson¹,

Abboud²,

Mark³

1985

J. Clin. Invest.

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We studied the contribution of carotid vs. extracarotid baroreceptors in control of heart rate in normal humans. We measured heart interval (HI) and arterial pressure during steady-state infusion of phenylephrine (PE). PE increased mean arterial pressure (MAP) by 13±2 mmHg (mean±SEM; n = 10) and thus stimulated both carotid and aortic baroreceptors. Neck pressure (NP) was applied during PE infusion to counter the increase in transmural carotid sinus pressure, thus leaving only aortic baroreceptors stimulated by the increase in arterial pressure. PE infusion alone prolonged HI by 230±24 ms (P < 0.05). Application of NP attenuated the HI response to 65±22 ms above control (P < 0.05 vs. PE alone). During these steady-state increases in arterial pressure, elimination of the carotid baroreflex contribution reduced the HI prolongation by 41-70% in five subjects and by >93% in five subjects.We also measured the HI response to dynamic ramp elevation of systolic arterial pressure (SAP) using bolus administrations of PE. Baroreflex control was calculated from the slope of the regression correlating SAP to succeeding HI for PE alone (carotid and aortic baroreceptor activation) and for PE plus superimposed dynamic NP at levels equal to the increases in SAP (aortic baroreceptor activation). During PE alone, the baroreflex slope was 20.2±2.9 ms/mmHg (a = 10). During PE plus NP, the baroreflex slope was reduced by 30% to 14.1±2.8 ms/mmHg (P < 0.02 vs. during PE alone). Thus, during dynamic increases in arterial pressure, eliminating the carotid baroreflex contribution reduced the HI response by 30%.These studies indicate that extracarotid (presumably aortic) and carotid baroreflexes both participate in control of heart rate in humans. Extracarotid (aortic) baroreflexes appear to have the greater role in control of heart rate during dynamic increases in arterial pressure.

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“…The relative roles of carotid sinus and aortic baroreceptors in the reflex control of HR and vascular resistance during changes in arterial blood pressure have been investigated by denervation experiments in rabbits. 27 It was shown that reflex heart rate responses to PHE were impaired significantly by denervation of either carotid or aortic baroreceptors. In contrast, reflex vascular responses in the hindlimb (perfused at constant blood flow) were preserved except for a slight impairment of reflex vasoconstriction after aortic baroreceptor denervation.…”

Section: Effect Of Bcbr On Functional Baroreflex Performance During Vmentioning

confidence: 99%

Baroreflex Control of Muscle Sympathetic Nerve Activity After Carotid Body Tumor Resection

et al. 2003

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Abstract-Bilateral carotid body tumor resection causes a permanent attenuation of vagal baroreflex sensitivity. We retrospectively examined the effects of bilateral carotid body tumor resection on the baroreflex control of sympathetic nerve traffic. Muscle sympathetic nerve activity was recorded in 5 patients after bilateral carotid body tumor resection (1 man and 4 women, 51Ϯ11 years) and 6 healthy control subjects (2 men and 4 women, 50Ϯ7 years). Baroreflex sensitivity was calculated from changes in R-R interval and muscle sympathetic nerve activity in response to bolus injections of phenylephrine and nitroprusside. In addition, sympathetic responses to the Valsalva maneuver and cold pressor test were measured. The integrated neurogram of patients and control subjects contained a similar pattern of pulse synchronous burst of nerve activity. Baroreflex control of both heart rate and sympathetic nerve activity were attenuated in patients as compared with control subjects [heart rate baroreflex sensitivity: 3.68Ϯ0. 4,6,7 and carotid endarterectomy. 8 The resulting clinical syndrome of baroreflex failure is characterized by recurrent bouts of unrestrained sympathetic excitation, manifesting as severe hypertension, headache, and diaphoresis. The findings of excessive rises in plasma catecholamines during these attacks and of exaggerated pressor responses to cold and mental stress in these patients suggest the loss of baroreflexmediated inhibition of efferent sympathetic nerve activity. 4,6 In a previous study, we have demonstrated that although BCBR elicits the full-blown syndrome of baroreflex failure only in a minority of patients, 9 baroreflex control of heart rate is impaired and blood pressure variability is increased in the long term after BCBR. 9,10 Whether BCBR also affects baroreflex control of sympathetic outflow has not yet been established in humans.The aim of this study was to examine the chronic effects of BCBR on the baroreflex control of sympathetic nerve activity. In this cross-sectional, retrospective study of patients with BCBR and age-matched healthy control subjects, sympathetic baroreflex sensitivity was calculated from MSNA responses to (de-)activation of baroreceptors by phenylephrine and nitroprusside bolus injections. In addition, MSNA responses to the Valsalva maneuver and cold pressor test were assessed. Medical Center Nijmegen, the Netherlands, were included in this study. Individual information on tumor size, additional tumor localizations, and surgical details of these 5 patients are shown in the Table. The median interval between the second operation and the study was 6.7 years (range, 4.4 to 20.3 years). Patients were free of diabetes and neurological, cardiovascular, and pulmonary disease. Six healthy subjects (2 men and 4 women) served as control subjects. Full medical history and physical examination including blood pressure measurements revealed no abnormalities. Groups were matched for age (BCBR: 51.2Ϯ10.8 versus control subjects: 50.0Ϯ6.5 years), body mass index (24.8Ϯ1.1 ve...

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Differential baroreflex control of heart rate and vascular resistance in rabbits. Relative role of carotid, aortic, and cardiopulmonary baroreceptors.

Cited by 93 publications

References 44 publications

Arterial baroreflex control of sympathetic nerve activity during elevation of blood pressure in normal man: dominance of aortic baroreflexes.

Arterial baroreflex control of sympathetic nerve activity during elevation of blood pressure in normal man: dominance of aortic baroreflexes.

Relative contribution of aortic and carotid baroreflexes to heart rate control in man during steady state and dynamic increases in arterial pressure.

Baroreflex Control of Muscle Sympathetic Nerve Activity After Carotid Body Tumor Resection

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