The mechanism of the inotropic effect of a reduction of extracellular potassium from 5.4 to 2.7 mM was investigated in myocytes isolated from guinea-pig ventricle. Action potentials were recorded using intracellular microelectrodes and cell shortening was measured by analysis of a video image. Changes in cytosolic calcium transients were estimated from calcium-activated currents under voltage-clamp conditions. The aim was to determine whether the prolongation of action potential duration which was observed to occur in low potassium might contribute to the increased shortening and increase in calcium-activated current under these conditions. Using a voltage-clamp waveform to mimic the waveform of the action potential, it was found that reduction of potassium caused a marked increase in cell shortening and of calcium-activated current in the absence of prolongation of the 'action potential' waveform. No change in inward calcium current was detected when extracellular potassium was reduced. The sensitivity to strophanthidin appeared to be increased under these conditions. We conclude that prolongation of the action potential is not a major factor contributing to the increased cell shortening and to the increased cytosolic calcium transient when extracellular potassium is reduced.