Modulation of contractility in failing human myocytes by reverse-mode Na/Ca exchange.
A decrease in the peak systolic [Ca](i) and slow decay of the Ca(i) transient are common features of the end-stage failing human ventricular myocyte and may underlie the contractile abnormalities observed in congestive heart failure. The role of the Na/Ca exchanger has been a great area of interest given the changes observed at the molecular level. Results from these experiments have been inconsistent, however, and therefore cellular-based experiments may be required to characterize the role of the Na/Ca exchanger in failing human myocardium. We review recent data that suggest an increased ability of the Na/Ca exchanger to transport Ca into the cytoplasm in failing human myocytes. We hypothesize that this increased Ca influx can explain the slowed decay and impaired relaxation of failing human ventricular myocytes.
Piacentino
Valentino
V
Department of Physiology, Temple University, Philadelphia, Pennsylvania 19140, USA.
Weber
Christopher R
CR
Gaughan
John P
JP
Margulies
Kenneth B
KB
Bers
Donald M
DM
Houser
Steven R
SR
D000818:Animals; D002118:Calcium / Q000378:metabolism; D006333:Heart Failure / Q000503:physiopathology*; D006352:Heart Ventricles; D006801:Humans; D032342:Muscle Cells / Q000502:physiology*; D009200:Myocardial Contraction / Q000502:physiology*; D012964:Sodium / Q000378:metabolism; D019831:Sodium-Calcium Exchanger / Q000502:physiology*
D019831:Sodium-Calcium Exchanger; D012964:Sodium; D002118:Calcium