EC-coupling in normal and failing hearts

Systolic heart failure may be due to too few cardiomyocytes, or to reduced contractile function of the heart cells. In the latter situation the myocardial function is impaired and this condition is called myocardial failure. The pathophysiological mechanism behind this cellular defect is not known,...

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Bibliographic Details
Published in:International journal of food sciences and nutrition 2005-04, Vol.39 (1-2), p.13-23
Main Authors: Birkeland, Jon Arne, Sejersted, Ole M., Taraldsen, Tore, Sjaastad, Ivar
Format: Article
Language:English
Subjects:
Action Potentials
Animals
Calcium Signaling
Calcium-Transporting ATPases - metabolism
Electrophysiology
excitation-contraction coupling
Female
Heart failure
Heart Failure - etiology
Heart Failure - physiopathology
Humans
Male
Myocardial Contraction - physiology
myocardial failure
Myocytes, Cardiac - cytology
Sarcoplasmic Reticulum - physiology
Sensitivity and Specificity
Sodium-Calcium Exchanger - metabolism
Ventricular Dysfunction, Left - etiology
Ventricular Dysfunction, Left - physiopathology
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Summary:Systolic heart failure may be due to too few cardiomyocytes, or to reduced contractile function of the heart cells. In the latter situation the myocardial function is impaired and this condition is called myocardial failure. The pathophysiological mechanism behind this cellular defect is not known, but Ca2+ handling is altered. Although the most important trigger of sarcoplasmatic reticulum (SR) Ca2+ release, the L-type Ca2+ current, seems to be unaltered, SR Ca2+ load is reduced in human heart failure. This could explain the reduced contractility observed in failing hearts. Three possible mechanisms have been suggested to explain the reduction in SR Ca2+ load. They are leak through the SR Ca2+ release channel (RyR), impaired SR Ca2+ ATPase (SERCA) function and increased Na+/Ca2+-exchanger (NCX) function. Leak through RyR is not consistently found. Increased NCX function is probably secondary to a change in Ca2+ handling, and thus not a primary mechanism, but blockade of the NCX might have therapeutic potential. Reduced SERCA function is probably a primary mechanism for the observed systolic dysfunction, and further insight is to be gained through studies in genetically modified models.
ISSN:0963-7486
1401-7431
1465-3478
1651-2006
DOI:10.1080/14017430410004632