Document Detail


Mechanoelectrical feedback: role of beta-adrenergic receptor activation in mediating load-dependent shortening of ventricular action potential and refractoriness.
MedLine Citation:
PMID:  11468214     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Augmented preload increases myocardial excitability by shortening action potential duration (APD). The mechanism governing this phenomenon is unknown. Because myocardial stretch increases intracellular cAMP, we hypothesized that load-dependent changes in myocardial excitability are mediated by beta-adrenergic stimulation of a cAMP-sensitive K(+) current. METHODS AND RESULTS: The effects of propranolol on load-induced changes in electrical excitability were studied in 7 isolated ejecting canine hearts. LV monophasic APD at 50% and 90% repolarization (MAPD(50) and MAPD(90)) and refractoriness were determined at low (9+/-3 mL) and high (39+/-4 mL) load before and after beta-adrenergic blockade. During control, the MAPD(50) decreased from 193+/-26 to 184+/-26 ms with increased load, as did the MAPD(90) (238+/-28 to 233+/-28 ms), P</=0.04. Similar changes were observed in ventricular refractoriness. Treatment with propranolol completely abolished these load-induced effects. Myocardial catecholamine depletion with reserpine in 2 hearts also abolished changes in MAPD and excitability in response to increased preload. CONCLUSIONS: Increases in ventricular load mediate a decrease in ventricular APD and refractoriness through activation of the beta-adrenergic receptor. An increase in a cAMP-mediated K(+) current, possibly the slowly activating delayed rectifier I(Ks), may account in part for this form of mechanoelectrical coupling.
Authors:
B B Lerman; E D Engelstein; D Burkhoff
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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:  Circulation     Volume:  104     ISSN:  1524-4539     ISO Abbreviation:  Circulation     Publication Date:  2001 Jul 
Date Detail:
Created Date:  2001-07-24     Completed Date:  2001-09-06     Revised Date:  2008-11-21    
Medline Journal Info:
Nlm Unique ID:  0147763     Medline TA:  Circulation     Country:  United States    
Other Details:
Languages:  eng     Pagination:  486-90     Citation Subset:  AIM; IM    
Affiliation:
Department of Medicine, Division of Cardiology, The New York Hospital-Cornell University Medical Center, New York, NY, USA.
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MeSH Terms
Descriptor/Qualifier:
Action Potentials / drug effects*
Adrenergic Uptake Inhibitors / pharmacology
Adrenergic beta-Antagonists / pharmacology*
Animals
Biomechanics
Dogs
Electrophysiology
Feedback / physiology
Heart Ventricles / drug effects*,  physiopathology
Propranolol / pharmacology*
Receptors, Adrenergic, beta / metabolism,  physiology*
Reserpine / pharmacology
Ventricular Function
Ventricular Pressure / drug effects
Grant Support
ID/Acronym/Agency:
R01-HL-56139/HL/NHLBI NIH HHS; R29-HL-51885/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Adrenergic Uptake Inhibitors; 0/Adrenergic beta-Antagonists; 0/Receptors, Adrenergic, beta; 50-55-5/Reserpine; 525-66-6/Propranolol

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


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