A Possible Role for Intracellular Sodium Ions in the Control of Contraction in Frog Atrial Trabeculae by Way of the Sodium‐calcium Exchange

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 . 1-1 to 10 mumol . l-1) and to the ionophore monensin (10 nmol . l-1 to 100 mumol . 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 mumol . 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 by 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.