A POSSIBLE ROLE FOR INTRACELLULAR SODIUM IONS IN THE CONTROL OF CONTRACTION IN FROG ATRIAL TRABECULAE BY WAY OF THE SODIUM-CALCIUM EXCHANGE

¹ Department of Physiology, University of Leicester, Leicester LE1 7RH

The effect of various inotropic agents on the strength of the Na-withdrawal contracture of isolated frog atrial trabeculae has been determined. Increasing the heart rate (0·1 min^-1 to 40 min^-1), exposure to low external K concentration ([K]_o) (1-0·3 mmol.l^-1), to strophanthidin (10 nmol.l^-1 to 10 µmol.l^-1) and to the ionophore monensin (10 nmol.l^-1 to 100 µmol.l^-1) all cause a progressive increase in the strength of the Na-withdrawal contracture, so that the curve relating external Na concentration ([Na]_o) to contracture tension is shifted towards higher values of [Na]_o. By contrast adrenaline (1 nmol.l^-1 to 1 µmol.l^-1) causes a decrease in the strength of Na-withdrawal contractures. As increased heart rate, the application of K-depleted fluids, strophanthidin or monensin are likely to increase internal Na concentration ([Na]_i), the change in relationship between [Na]_o and contracture tension can be fitted using equations for a 3 Na⁺ for 1 Ca²⁺ exchange and for pCa vs. relative tension, by varying the apparent [Na]_i. The increased Na influx necessary to change [Na]_i by the amount suggested b---y these calculations agrees well with direct measurements made by other workers. A similar relationship is observed between the strength of the heart beat and the calculated [Na]_i for the effects of increased heart rate, the application of strophanthidin, low [K]_o or monensin. The effects of adrenaline, however, cannot be interpreted in the same way, suggesting that at least one other process mediates the strength of the heart beat. Various possibilities are discussed.