Document Detail


Baroreflex control of muscle sympathetic nerve activity in borderline hypertension.
MedLine Citation:
PMID:  2394007     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Patients with borderline hypertension have exaggerated vascular responses to orthostatic stress produced by tilt or lower body negative pressure (LBNP). It has been suggested that 1) in the supine position, these patients have augmented activity of cardiopulmonary baroreceptors that exerts an increased restraint on sympathetic vasoconstrictor tone; 2) withdrawal of this augmented inhibitory baroreceptor activity during orthostatic stress elicits augmented reflex sympathetic vasoconstrictor outflow; and 3) augmented cardiopulmonary baroreceptor activity may be secondary to impaired arterial baroreflex mechanisms. To test these hypotheses, we recorded muscle sympathetic nerve activity from the peroneal nerve in seven borderline hypertensive subjects and seven age-, sex-, and weight-matched normotensive subjects during three levels of nonhypotensive LBNP and infusions of phenylephrine and nitroprusside. During LBNP, reductions of central venous pressure were similar in borderline hypertensive and normotensive subjects, and arterial pressure and heart rate values were unchanged. Increases of sympathetic nerve activity, however, were significantly greater in borderline hypertensive than in normotensive subjects at each level of LBNP, indicating an augmented gain of the cardiopulmonary baroreflex. To determine whether this augmentation is related to impairment of arterial baroreflexes, we measured changes of sympathetic nerve activity during increases and decreases of arterial pressure produced with infusions of intravenous phenylephrine and nitroprusside. Central venous pressure was held at control levels by LBNP during phenylephrine and saline infusion during nitroprusside. Changes of sympathetic nerve activity during alterations of arterial pressure were similar in borderline hypertensive and normotensive subjects. These data show that cardiopulmonary baroreflex control of SNA is augmented in borderline hypertensive subjects and that this augmentation does not result from an attenuation of the arterial baroreflex.
Authors:
R F Rea; M Hamdan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Circulation     Volume:  82     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1990 Sep 
Date Detail:
Created Date:  1990-10-09     Completed Date:  1990-10-09     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  856-62     Citation Subset:  AIM; IM; S    
Affiliation:
Department of Internal Medicine, University of Iowa, Iowa City 52242.
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MeSH Terms
Descriptor/Qualifier:
Blood Pressure
Central Venous Pressure
Humans
Hypertension / physiopathology*
Lower Body Negative Pressure
Male
Muscles / innervation,  physiopathology*
Nitroprusside / diagnostic use
Phenylephrine / diagnostic use
Pressoreceptors / physiopathology*
Reference Values
Sympathetic Nervous System / physiopathology*
Chemical
Reg. No./Substance:
15078-28-1/Nitroprusside; 59-42-7/Phenylephrine
Comments/Corrections
Comment In:
Circulation. 1990 Sep;82(3):1057-9   [PMID:  2393992 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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