INVOLVEMENT OF THE SARCOPLASMIC-RETICULUM CALCIUM-PUMP IN MYOCARDIAL CONTRACTILE DYSFUNCTION - COMPARISON BETWEEN CHRONIC PRESSURE-OVERLOADAND STUNNING

Acute as well as chronic forms of heart failure involve mechanical dys function during systole and/or diastole. The rapid Ca2+ release from a nd Ca2+ reuptake into the tubuli of the sarcoplasmic reticulum are pro cesses that critically determine normal systolic and diastolic myocard ial function, which explains why in the last fifteen years so much att ention has been paid to understand the performance of the sarcoplasmic reticulum Ca2+ pump during myocardial contractile dysfunction. In thi s communication pie have reviewed the literature data on sarcoplasmic reticulum Ca2+ pump function in the chronically pressure-overloaded hy pertrophied and stunned (post-ischemic reversibly injured) myocardium in the light of some new data from our laboratory. Results on the pres sure-overloaded hypertrophied myocardium provide evidence that impaire d relaxation is most likely due to a low capacity of the sarcoplasmic reticulum to pump Ca2+, a consequence of a lower density of Ca2+-pumpi ng sites within the sarcotubular membranes. Contractile dysfunction in stunned myocardium is accompanied by an upregulation of the sarcoplas mic reticulum Ca2+ ATPase gene resulting in a slight increase of the C a2+ pumping activity. The latter increase is likely an adaptive respon se of the reversibly injured myocardium which may contribute to the sl ow recovery of contractile function.