Journal article
Arterial Baroreflexes in Renal Hypertensive Rabbits: Selectivity and Redundancy of Baroreceptor Influence on Heart Rate, Vascular Resistance, and Lumbar Sympathetic Nerve Activity
Circulation research, Vol.53(2), pp.223-234
08/1983
DOI: 10.1161/01.RES.53.2.223
PMID: 6883646
Abstract
The first purpose of this study was to determine if the baroreflex control of hindlimb resistance is preserved in hypertension even though reflex control of heart rate is impaired. The second purpose was to compare the capacity of one remaining set of arterial baroreceptors to compensate for the loss of the other in normotensive and hypertensive states. Baroreflex responses of heart rate, perfusion pressure in the hindlimb (perfused at constant flow), and lumbar sympathetic nerve activity were examined in rabbits anesthetized with chloralose and urethane 6 weeks after induction of renal hypertension (1-K-l-W). Intravenous injections of phenylephrine caused increases in arterial pressure and reflex bradycardia, vasodilarion, and inhibition of lumbar sympathetic nerve activity. The converse occurred with nirroglycerin. With all baroreceptors intact, baroreflex control of heart rate was impaired in hypertensive rabbits, whereas control of vascular resistance and lumbar sympathetic nerve activity was preserved in hypertensive as compared with normotensive sham-operated rabbits. Denervation of either the carotid sinus or aortic baroreceptors in normotensive rabbits resulted in the following(a) reflex control of heart rate with phenylephrine and nitroglycerin was impaired; (b) reflex inhibition of lumbar sympathetic nerve activity was preserved and reflex vasodilation was augmented; and (c) reflex excitation of lumbar sympathetic nerve activity was reduced but reflex vasoconstriction was preserved after section of carotid sinus baroreceptors and reduced slightly after section of aortic baroreceptors. In hypertensive rabbits, section of carotid sinus or aortic baroreceptors resulted in the following(a) reflex control of heart rate was markedly impaired; (b) reflex inhibition of lumbar sympathetic nerve activity and vasodilation were suppressed; and (c) reflex excitation and vasoconstriction were impaired to a much greater extent than in normotensives. Our conclusions are as follows. (1) Baroreflex control of hindlimb vascular resistance and lumbar sympathetic nerve activity is preserved in hypertension, even though control of heart rate is impaired. Therefore, impaired baroreflex control of heart rate cannot be taken as evidence of a generalized impairment of baroreflex control of vascular resistance, (2) In normotensives, one remaining set of arterial baroreceptors compensates for the loss of the other in the reflex regulation of hindlimb vascular resistance and in reflex inhibition of lumbar sympathetic nerve activity but not in the regulation of heart rate. Thus, there is a ‘redundancy’ in the arterial baroreflex control of hindlimb resistance and lumbar sympathetic nerve activity but not in the control of heart rate, (3) This compensatory capacity or ‘redundancy’ of baroreflex control is significantly impaired in renal hypertensive rabbits, and the impairment may be related to impaired baroreceptors or abnormal central mediation of the reflex.
Details
- Title: Subtitle
- Arterial Baroreflexes in Renal Hypertensive Rabbits: Selectivity and Redundancy of Baroreceptor Influence on Heart Rate, Vascular Resistance, and Lumbar Sympathetic Nerve Activity
- Creators
- Gary Guo - Cardiovascular Division, Department of Internal Medicine, and Department of Physiology, Cardiovascular Center, The University of Iowa College of Medicine, Iowa City, IowaMarc ThamesFrancois Abboud
- Resource Type
- Journal article
- Publication Details
- Circulation research, Vol.53(2), pp.223-234
- Publisher
- American Heart Association, Inc
- DOI
- 10.1161/01.RES.53.2.223
- PMID
- 6883646
- ISSN
- 0009-7330
- eISSN
- 1524-4571
- Language
- English
- Date published
- 08/1983
- Academic Unit
- Molecular Physiology and Biophysics; Cardiovascular Medicine; Fraternal Order of Eagles Diabetes Research Center; Internal Medicine
- Record Identifier
- 9984025591502771
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