Document Detail

Accentuated antagonism in the control of human heart rate.
MedLine Citation:
PMID:  10954067     Owner:  NLM     Status:  MEDLINE    
Invasive animal models indicate that the accelerative effects of the sympathetic nervous system on heart rate are highly dependent on the background level of vagal activity. A noninvasive, parasympathetic chronotropic index (respiratory sinus arrhythmia) and a sympathetic chronotropic index (left ventricular ejection time) were used to evaluate autonomic control of human heart rate. A strong interaction, previously called accentuated antagonism, was found. Sympathetic heart rate effects were substantially smaller with high levels of vagal tone than with low vagal background activity. Furthermore, vagal effects became progressively stronger with increasing sympathetic background activity, demonstrating the predominance of parasympathetic control of human heart rate. This finding implies that changes in cardiac activity resulting from changes in sympathetic control cannot be interpreted accurately unless concurrent vagal activity is taken into account, as well.
S H Uijtdehaage; J F Thayer
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Clinical autonomic research : official journal of the Clinical Autonomic Research Society     Volume:  10     ISSN:  0959-9851     ISO Abbreviation:  Clin. Auton. Res.     Publication Date:  2000 Jun 
Date Detail:
Created Date:  2000-12-04     Completed Date:  2000-12-14     Revised Date:  2004-11-17    
Medline Journal Info:
Nlm Unique ID:  9106549     Medline TA:  Clin Auton Res     Country:  ENGLAND    
Other Details:
Languages:  eng     Pagination:  107-10     Citation Subset:  IM    
Department of Psychiatry and Behavioral Sciences, University of California, Los Angeles, USA.
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MeSH Terms
Arrhythmia, Sinus / physiopathology
Heart Conduction System / physiology*
Heart Rate / physiology*
Models, Cardiovascular
Parasympathetic Nervous System / physiology*
Sympathetic Nervous System / physiology*
Ventricular Function, Left

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