Using standard microelectrode techniques, the effects of strontium (Sr++) ions on action potential (AP) repolarizations in rabbit sinoatrial node (SAN) cells were studied. In a nominally magnesium-free, calcium-free solution, Sr++ (0.5-3.55 mmol) produced an early afterdepolarization (EAD) and a prolongation of the AP. Until now, no experimental evidence has been presented in favor of an EAD mechanism in SAN cells. Superfusion of the SAN cells with 0.5 mmol Sr++ solution containing 1-5 mmol magnesium (Mg++) or 0.5 mmol calcium (Ca++) did not induce the EAD. Increasing the extracellular Mg++ to 1-5 mmol did not affect the EAD induced by superfusion with 3.55 mmol Sr++ solution. Increasing the extracellular Ca++ to 0.5 mmol suppressed the 3.55 mmol Sr(++)-induced EAD. The presence of 0.3 mmol manganese (Mn++) suppressed the EAD induced by superfusion with 0.5 mmol Sr++ solution. The EAD did not occur in the presence of 1 x 10(-6) mol nitrendipine or 2 x 10(-6) mol diltiazem hydrochloride. The presence of 0.03 mmol Mn++ did not significantly alter the 0.5 mmol Sr(++)-induced EAD. These results suggest that a slow inward Sr++ current through the Ca++ channel has an important role in the development of the EAD.