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Sarcoplasmic Reticulum Proteins in Heart Failure
Author(s) -
LEHNART STEPHAN E.,
SCHILLINGER WOLFGANG,
PIESKE BURKERT,
PRESTLE JÜRGEN,
JUST HANJÖRG,
HASENFUSS GERD
Publication year - 1998
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.1998.tb08270.x
Subject(s) - calsequestrin , phospholamban , endoplasmic reticulum , medicine , calcium , endocrinology , heart failure , sodium calcium exchanger , chemistry , calcium atpase , homeostasis , atpase , diastole , ryanodine receptor , biology , biochemistry , enzyme , blood pressure
Altered calcium homeostasis may play a key role in the pathophysiology of human heart failure. Levels of sarcoplasmic reticulum (SR) proteins and sarcolemmal Na + ‐Ca 2+ exchanger were analyzed by Western blot in failing and nonfailing human myocardium and related to myocardial function. Levels of the SR calcium release channel and of calcium storage proteins (calsequestrin and calreticulin) were not different in nonfailing and failing hearts. However, proteins involved in calcium removal were significantly altered in the failing human heart: (1) SR‐Ca 2+ ‐ATPase levels and the ratio of SR‐Ca 2+ ‐ATPase to its inhibitory protein phospholamban were significantly decreased, and (2) Na + ‐Ca 2+ exchanger levels and the ratio of Na + ‐Ca 2+ exchanger to SR‐Ca 2+ ‐ATPase were significantly increased. SR‐Ca 2+ ‐ATPase levels were closely correlated to systolic function as evaluated by frequency potentiation of contractile force. The frequency‐dependent rise of diastolic force was inversely correlated with protein levels of Na + ‐Ca 2+ exchanger. These findings indicate that altered expression of SR‐Ca 2+ ‐ATPase and Na + ‐Ca 2+ exchanger is relevant for altered systolic and diastolic function in human heart failure.