Functional properties of failing human ventricular myocytes.
Reduced peak systolic Ca2+ and slow decay of the Ca2+ transient are common features of the end-stage failing human ventricular myocyte and are thought to underlie abnormal ventricular contractility in congestive heart failure (CHF). Individual changes in the expression or activity of Ca2+ transport proteins of the sarcoplasmic reticulum (SR Ca2+ ATPase, SERCa) or the sarcolemmal (sodium-calcium exchanger, NCX) have not always been observed in CHF and cannot per se consistently explain these Ca2+ transient defects. We review recent data that suggests that the normal balance of transport activities of SERCa and NCX is deranged in failing human myocytes. We hypothesize that an increase in the NCX/SERCa transport capacity in failing myocytes can explain the abnormal Ca2+ homeostasis of the failing human ventricular myocyte.
Houser
S R
SR
Cardiovascular Research Group, Molecular and Cellular Cardiology Laboratories, Temple University School of Medicine, 3400 North Broad Street, Philadelphia, PA 19140, USA. srhouser@unix.temple.edu
Piacentino
V
V
Mattiello
J
J
Weisser
J
J
Gaughan
J P
JP
D000200:Action Potentials; D002118:Calcium / Q000378:metabolism*; D000252:Calcium-Transporting ATPases / Q000378:metabolism; D004558:Electric Stimulation; D006333:Heart Failure / Q000378:metabolism / Q000503:physiopathology*; D006706:Homeostasis; D006801:Humans; D009200:Myocardial Contraction / Q000502:physiology; D009206:Myocardium / Q000378:metabolism*; D012519:Sarcoplasmic Reticulum / Q000378:metabolism; D019831:Sodium-Calcium Exchanger / Q000378:metabolism
D019831:Sodium-Calcium Exchanger; D000252:Calcium-Transporting ATPases; D002118:Calcium