The sarcolemmal mechanisms involved in the control of diastolic intracellular calcium in isolated rat cardiac trabeculae

We performed experiments using the calcium indicator Indo-1 to determine the relative roles of the sarcolemmal mechanisms involved in the regulation of diastolic intracellular calcium concentration ([Ca2+](i)) in trabeculae from the rat heart. Ryanodine was used to eliminate sarcoplasmic reticulum (SR) function. In the functional absence of the SR, 76.8 ± 3.9% of the calcium was extruded by the Na-Ca exchange carrier in the [Ca2+](i) range of diastolic concentration ± 200-400 nM. This was assessed by measuring the recovery of [Ca2+](i) from small perturbations in the presence and absence of extracellular sodium. The steady-state relationship between [Ca2+](o) and [Ca2+](i) was linear over the range of 1-40 mM, a 20-fold increase of [Ca2+](o) produced a 1.97-fold ± 0.13-fold increase in [Ca2+](i) (n = 5). In the absence of extracellular sodium raising [Ca2+](o) had a variable effect. In some preparations there was little change of [Ca2+](i) while in others the response was almost as large as in control conditions. We conclude that the Na-Ca exchanger contributes ~77% of sarcolemmal calcium extrusion following small perturbations in [Ca2+](i) and that this fraction does not diminish as the [Ca2+](i) declines. In addition we have shown a sodium-independent entry of calcium into quiescent cardiac muscle under resting conditions.