Abstract
Myocardial contractile dysfunction in congestive heart failure is characterized by a decrease in force developed and retardation of relaxation. These alterations are mainly due to those in intracellular Ca(2 +) transients (CaT) . CaT are regulated by a number of functional proteins, including sarcolemmal L-type Ca(2 +) channels, Na(+)/Ca(2 +) exchanger and Ca(2 +) ATPase, sarcoplasmic reticulum Ca(2 +) ATPase (SERCA 2 ) , phospholamban and ryanodine receptors, and mitochondrial Ca(2 +) uniporter. Changes in expression and function of these regulatory proteins that occur in the course of increasing severity of heart failure are responsible for the characteristic changes in force development and relaxation observed under pathophysiological conditions in congestive heart failure.
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