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 determi ne the relative roles of the sar colemmal mechanisms involved in the r egulation of diastolic intracellular calcium concentration ([Ca2+](i)) in trabeculae from the rat heart. Ryanodine was used to eliminate sar coplasmic reticulum (SR) function. In the functional absence of the SR , 76.8 +/- 3.9% of the calcium was extruded by the Na-Ca exchange carr ier in the [Ca2+](i) range of diastolic concentration +/- 200-400 nM. This was assessed by measuring the recovery of [Ca2+](i) from small pe rturbations in the presence and absence of extracellular sodium. The s teady-state relationship between [Ca2+](o) and [Ca2+](i) was linear ov er 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 th at the Na-Ca exchanger contributes approximate to 77% of sarcolemmal c alcium extrusion following small perturbations in [Ca2+](i) and that t his fraction does not diminish as the [Ca2+](i) declines. In addition we have shown a sodium-independent entry of calcium into quiescent car diac muscle under resting conditions.