Document Detail


Postexcitatory depression of baroreceptors in dogs with experimental heart failure.
MedLine Citation:
PMID:  1849369     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The phenomenon of postexcitatory depression (PED) of baroreceptors is related to augmentation of Na(+)- K(+) -adenosinetriphosphatase (ATPase) activity. To provide additional evidence to support the hypothesis that dogs with chronic heart failure have augmented Na(+) -K(+) -ATPase activity in baroreceptor endings, the present study was undertaken to compare the duration of the PED of carotid sinus baroreceptors from normal and heart failure dogs. The effect of perfusion of the carotid sinus with a cardiac glycoside was also investigated. Eight normal and six dogs with experimental heart failure induced by ventricular pacing (250 beats/min for approximately 5 wk) were used in this study. Dogs were anesthetized, and the carotid sinus was isolated and perfused. Single baroreceptor units from the carotid sinus nerve were recorded, and the duration of the PED was measured. The relationship between the magnitude of the pressure steps and the duration of PED was determined. Duration of PED was significantly prolonged in the heart failure group at each pressure step (range from 2.7 to 9.0 s compared with 0.5 to 2.9 s in normal dogs). For the relationship between the duration of the pressure step and duration of PED, the heart failure dogs exhibited a markedly longer duration of PED than the normal dogs (range from 2.3 to 12.4 s compared with 0.5 to 5.3 s in normal dogs). Perfusion of the carotid sinus with very low doses of ouabain decreased the duration of PED in the heart failure dogs; however, there was no such effect in the normal dogs. These data are consistent with the view that baroreceptor membranes have increased Na(+) -K(+) -ATPase activity in heart failure(ABSTRACT TRUNCATED AT 250 WORDS)
Authors:
W Wang; J S Chen; I H Zucker
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The American journal of physiology     Volume:  260     ISSN:  0002-9513     ISO Abbreviation:  Am. J. Physiol.     Publication Date:  1991 Apr 
Date Detail:
Created Date:  1991-05-09     Completed Date:  1991-05-09     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370511     Medline TA:  Am J Physiol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  H1160-5     Citation Subset:  IM    
Affiliation:
Department of Physiology and Biophysics, University of Nebraska, College of Medicine, Omaha 68198-4575.
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MeSH Terms
Descriptor/Qualifier:
Animals
Cardiac Output
Carotid Sinus / physiopathology
Dogs
Female
Heart Failure / physiopathology*
Heart Rate
Heart Ventricles / physiopathology
Hemodynamics
Male
Ouabain / pharmacology
Pressoreceptors / physiopathology*
Pressure
Sodium-Potassium-Exchanging ATPase / metabolism
Grant Support
ID/Acronym/Agency:
HL-39690/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
630-60-4/Ouabain; EC 3.6.3.9/Sodium-Potassium-Exchanging ATPase

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


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