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 hypothesized 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.