It already has been well documented that the maximum rate of depolarization and amplitude of action potentials are directly dependent on [Na+]o in the vertebrate myocardium. Almost all studies have been carried out at low sodium concentration ranges by substituting NaCl for other substances. Action potentials should be demonstrable in higher sodium concentrations, but cells are inevitably damaged by osmotic changes. The blood of elasmobranchs is nearly isosmotic with sea water, but NaCl accounts for 54.5% of the osmotic pressure and 38.7% of it is maintained by urea molecules. Utilizing this special situation in elasmobranchs, the effect of high sodium concentration was studied up to 170% of normal sodium concentration, while still retaining isosmotic condition. The rate of depolarization, amplitude, and duration of the myocardial action potential all increased in direct proportion to [Na+]o, and no depressant effect on transmembrane action potentials was observed in solutions of high sodium concentration. With regard to depolarization rate, the regression curve fitted by the least squares method passed through zero within two standard errors. At high sodium levels, the overshoot changed as expected theoretically, but at lower ranges it deviated from the theoretical values. [Na+]i and [K+]i in this tissue have been determined, and these data are explained on the basis of the Na theory.