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.