Document Detail


Baroreceptor function in congestive heart failure: effect on neurohumoral activation and regional vascular resistance.
MedLine Citation:
PMID:  2882866     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
A series of neurohumoral systems are activated in congestive heart failure that contribute to the increased vascular resistance and sodium retention that characterize this disorder. Abnormalities in baroreceptor function are intrinsic to the pathophysiology of heart failure and may subserve the vasoconstrictive and volume overloaded state that defines patient morbidity. Blunted baroreceptor responses to high cardiac filling pressures or depressed cardiac function reduce afferent signals that normally inhibit sympathetic efferent activity, vasopressin release, and indirectly, renin secretion. The resulting increase in neurohumoral activity mediates the redistribution of blood flow that occurs in this disorder. Limb blood flow is usually reduced and may be responsible for exercise intolerance. Decreased renal blood flow and altered intrarenal hemodynamics contribute to sodium retention. In addition, renal vasoconstriction and elevated circulating levels of angiotensin II and vasopressin may contribute to hyponatremia by influencing free water intake and excretion. Hence, baroreceptor dysfunction may be a principal mechanism that contributes to neurohumoral activation and subsequent alteration in vascular resistance and sodium and water balance in congestive heart failure. It may not be coincidental that two principal markers of an unfavorable prognosis in patients with heart failure, high plasma norepinephrine levels and hyponatremia, share baroreceptor dysfunction as a common theme.
Authors:
A T Hirsch; V J Dzau; M A Creager
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Circulation     Volume:  75     ISSN:  0009-7322     ISO Abbreviation:  Circulation     Publication Date:  1987 May 
Date Detail:
Created Date:  1987-06-01     Completed Date:  1987-06-01     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  IV36-48     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Heart Failure / physiopathology*
Humans
Neurotransmitter Agents / physiology*
Pressoreceptors / physiopathology*
Regional Blood Flow*
Vascular Resistance*
Chemical
Reg. No./Substance:
0/Neurotransmitter Agents

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


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