CALCIUM-CONCENTRATION AND MOVEMENT IN THE VENTRICULAR CARDIAC CELL DURING AN EXCITATION-CONTRACTION CYCLE

This paper extends the model for Ca movement in the cardiac ventricula r cell from the diadic cleft space to the entire sarcomere. The model predicts the following: 1) Shortly after SR release there is a [Ca] gr adient >3 orders of magnitude from cleft center to M-line which, 50 ms after release, is still >30. Outside the cleft, 40 ms after cessation of release, the axial gradient from Z to M-line is >3. 2) At the end of SR release, >50% of the total Ca released is bound to low-affinity inner sarcolemmal phospholipid binding sites within the cleft. 3) Halv ing the SR release almost doubles the fraction of release removed from the cell via Na/Ca exchange and reduces average sarcomeric free [Ca] by 70%. 4) Adding 100 mu M fluo-3; Which doubles the buffering capacit y of the cytoplasm, reduces peak average sarcomeric [Ca] by >50% and i ncreases the initial half-time for [Ca] decrease by approximately twof old. 5) A typical Ca ''spark'' can be generated by an SR release 20% o f maximum (4 x 10(-20) moles) over 2 ms. Fluo-3 (100 mu M) significant ly ''shrinks'' the spark. 6) The ''spark'' isa consequence of elementa ry events within the diadic cleft space. For example, removal of cleft binding;sites would cause average sarcomeric Ca to increase by >10 fo ld, fall 10 times more rapidly, decrease latency for appearance of the spark by >20 times, and reduce spark duration by 85%. 7) Dividing SR Ca release between cleft and corbular SR produces a secondary [Ca] pea k and a ''flattening'' of the sarcomeric [Ca] transient. These changes probably could not be resolved with current confocal microscopic tech niques.