Ca2+-handling in heart failure--a review focusing on Ca2+ sparks.
[Ca2+]i-transients have been shown to be altered in isolated ventricular myocytes from terminally failing human myocardium. It has been demonstrated that one reason for this alteration is a reduction in the Ca2+ content of the sarcoplasmic reticulum (SR). Further investigations were done to investigate, whether there may be an additional defect of the Ca2+-release mechanisms from the SR. These release mechanisms were investigated through the recording of Ca2+ sparks in single human myocytes. In cardiac myocytes, Ca2+ sparks are elementary units of Ca2+ release, which occur spontaneously, or which are triggered by Ca2+ influx through L-type Ca2+-channels (Ca2+-induced Ca2+ release). Ca2+ sparks have been investigated in various animal models of cardiac hypertrophy and cardiac failure and results were conflicting. Discrepancies may be explained by different species and also by the mechanisms underlying hypertrophy and heart failure. This review summarizes our current knowledge on Ca2+ sparks in heart failure.
Lindner
Michael
M
University of Cologne, Department of Medicine III, Joseph-Stelzmann-Str. 9, 50924 Cologne, Germany. michael.lindner@uni-koeln.de
Böhle
Thomas
T
Beuckelmann
Dirk J
DJ
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002303:Cardiac Output, Low / Q000378:metabolism*; D006801:Humans; D009206:Myocardium / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism
D002118:Calcium