Using the glass microelectrodes techniques, we analysed the causes of the shortening of the ventricular myocardial action potentials (AP) of albino rats during postnatal development. Delayed outward currents were blocked with tetraethylammonium (TEA) in 20 mmol.l-1 concentration. TEA led to prolongation of action potentials and to accentuation of frequency sensitivity in all the given age groups, but a block of TEA-sensitive currents nevertheless does not permit the conclusion that the cause of postnatal AP shortening is due to an increase in the intensity of outward currents. Slow inward current (Isi) were blocked with verapamil (2.10(-5) mol.l-1), which markedly shortened the myocardial AP of newborn rats; with advancing age its effect diminished and shifted to the negative membrane voltage level. The Isi was stimulated by adrenaline (10(-5) mol.l-1), which markedly prolonged the AP of newborn animals; with advancing age its effect rapidly diminished and was virtually undetectable in 10-day-old animals. The results indicate that postnatal AP prolongation is caused by a drop in the Isi rate rather than by the growth of outward repolarizing currents.