The effects of bathing sodium ions upon the intracellular sodium activity in calcium-free media and the calcium paradox of isolated ferret ventricular muscle.

Exposure of fine trabeculae isolated from the ferret right ventricle to media depleted of Ca2+, with a rapid perfusion system, causes a depolarization of the membrane and a rise in aiNa. This rise in aiNa is sigmoidally dependent upon the bathing free [Ca2+], is antagonized by reduction of the [Na]o, raised [Mg]o and PN200-110 but augmented by removal of Mg2+ or inhibition of the Na-pump. On repletion of Ca2+, the strength of the resulting contracture depends upon the transmembrane. Na-gradient at the moment of Ca-repletion. The effects of reduced [Na]o, during Ca-depletion, depend upon the cation used with replacement by Li much greater than choline greater than tetramethylammonium. These are determined by the change in the transmembrane gradient for Na+ and any additional action the replacing ion has upon the Ca-channels, the Na-pump and the Na/Ca exchange. The effects described are consistent with the hypothesis that the intensity of the calcium paradox in mammalian ventricle is primarily determined by the entry of Na+ through L-type Ca-channels during the period of Ca-depletion and the Ca-loading on Ca-repletion due to the effect of the raised aiNa upon the Na/Ca exchange.