The role of Ca++ ions in the hypertrophied myocardium [proceedings].
Pressure-hypertrophied right ventricular myocardium (RVH) demonstrates paradoxically increased oxygen consumption (MVO2) related to increased in vitro energy-linked mitochondrial calcium flux. The present experiments were designed to measure mitochondrial Ca++ retention in intact RVH and relate changes in mitochondrial Ca++ metabolism to altered RVH contractile behavior and relaxation. Sixteen cats were pulmonary artery banded and their hearts plus paired controls were perfused with 45Ca Krebs-Henseleit at 30 degrees C, 120 beats/min for 10 min. At Lmax papillary muscles showed reduced active tension, a slower contraction rate, a reduced relaxation rate, a greater time to peak tension and a greater relaxation time. Retained 45Ca of mitochondria was increased from 16.75 + .96nM/mg protein in controls to 20.82 +/- .98 in RVH, (p less than 0.005). This increase in mitochondrial 45Ca retention correlated (r equal to 0.93), (P less than 0.001) with the decreased rate of papillary muscle relaxation. These data show an increased 45Ca retention of mitochondria in pressure-induced RVH and relate this biochemical abnormality to a decreased myocardial relaxation in this state.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D006332:Cardiomegaly / Q000378:metabolism*; D002415:Cats; D006352:Heart Ventricles; D008931:Mitochondria, Muscle / Q000378:metabolism; D009200:Myocardial Contraction; D010101:Oxygen Consumption; D010210:Papillary Muscles / Q000378:metabolism
D002118:Calcium