Abstract

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 × 10 −6 mol nitrendipine or 2 × 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.

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