Na⁺/Ca²⁺ exchange and cell contraction in isolated neonatal and adult rabbit cardiac myocytes

Recent studies have demonstrated a relative deficiency in voltage-gated Ca²⁺ currents (I(Ca)) in immature myocardium. We hypothesi zed that contraction in developing heart results in part from Ca²⁺ influx via 'reverse' Na⁺/Ca²⁺ exchange current (I(Na/Ca)). Accordingly, I(Na/Ca) and cell contraction amplitude were measured in single neonatal and adult rabbit ventricular myocytes. I(Na/Ca) was dependent on Ca²⁺ concentration, Na⁺ concentration, and membrane potential and was blocked by 5 mM Ni²⁺ but not by the Ca²⁺-channel blocker nifedipine. In neonatal cells, contraction amplitude reached a plateau for depolarizations positive to 0 mV. In adult myocytes, contraction amplitude was maximal at 0 mV and decreased at positive membrane potentials. Inhibition of I(Ca) with nifedipine did not affect maximal contraction amplitude in neonatal myocytes but almost completely suppressed contraction of adult cells. These data suggest that Ca²⁺ influx via I(Ca) is not required for contraction of neonatal rabbit cardiac myocytes. Moreover, Ca²⁺ influx via reversal of the Na⁺/Ca²⁺ exchange mechanism may provide a significant portion of the Ca²⁺ regulating cell contraction, especially during depolarization to positive membrane potentials.