Aim: To study and compare the excitation-contraction coupling triggered by L-type calcium current and by reverse-mode Na/Ca exchange during depolarizing steps in single guinea-pig ventricular myocytes.
Methods: Whole-cell membrane-potential, membrane-current and cell-shortening data were simultaneously acquired during whole-cell voltage clamp protocols. Voltage clamp pulses elicited ICa(L) at + 10 mV, + 50 mV, + 100 mV and evoked contractions in myocytes superfused with Tyrode's solution at 35 degrees C.
Results: The greater the inhibition of I(Ca(L)), the more likely contractions would be abolished at +10 mV test potential. There was a correlation between them. At potential positive to + 50 mV, contractions were partially suppressed by Nif 100 micromol/L or Nif 30 micromol/L plus Cd2+30 micromol/L. The residual contraction was significantly delayed in onset. At +100 mV test potential, contractions were delayed in onset compare to + 50 mV and resistant to Nif 100 micromol/L or Nif 30 micromol/L plus Cd2+30 micromol/L. The residual contraction was completely blocked by Ni2+ at + 50 mV and + 100 mV.
Conclusions: I(Ca(L)) is the major trigger for excitation-contraction coupling. Na/Ca exchange modulates excitation-contraction coupling as both reverse and forward mode.