The role of intracellular sodium activity in the inotropy potentiation among high [Ca]o' norepinephrine and strophanthidin.

The mechanism by which high [Ca]o or norepinephrine potentiate the inotropic action of a low concentration of strophanthidin was investigated in cardiac Purkinje fibers perfused in vitro. The membrane potential, contractile force and intracellular sodium activity (aiNa) were recorded simultaneously and continuously. The following results were obtained. Increasing [Ca]o from 2.7 mM to 3.6 mM or administering norepinephrine (10(-7) M) increased the contractile force and decreased aiNa. Administration of a low concentration of strophanthidin (5 X 10(-8)M) increased the contractile force and aiNa. Occasionally, there was a transient small decrease in aiNa at the beginning of strophanthidin perfusion. When [Ca]o was increased in the presence of strophanthidin, aiNa decreased less and the contractile force increased more than in the absence of strophanthidin. Adding norepinephrine to the strophanthidin solution caused similar effects in that aiNa decreased less and contractile force more than in the absence of strophanthidin. The results suggest that the potentiation of the inotropic effect of strophanthidin by high [Ca]o or norepinephrine is due to the higher aiNa induced by strophanthidin and to the smaller decline in aiNa induced by high [Ca]o or norepinephrine.