Voltage dependence of sodium‐calcium exchange current in guinea‐pig atrial myocytes determined by means of an inhibitor.

Spontaneous transient inward currents (Iti) caused by cyclic release of Ca2+ ions from the sarcoplasmic reticulum were studied in cultured atrial myocytes from hearts of adult guinea-pigs. K+ channel currents were blocked by replacing K+ on both sides of the membrane by Cs+; the L-type Ca2+ current was inhibited by D600. 2. The voltage dependence of peak Iti and the background current displayed distinct outward-going rectification. The I-V curves for both currents approach each other at strongly positive membrane potentials but do not intersect. 3. 3'-4'Dichlorobenzamil (DCB) causes a concentration-dependent inhibition of peak Iti and a shift of the holding current (at -60 to -40 mV) in the inward direction. Inhibition of Iti is half-maximal at a concentration of 30 microM. 4. DCB reduces the outward-rectifying component of both peak Iti and the background current. The I-V curves of the control and DCB-inhibited currents intersect at ca. +10 mV (peak Iti) and negative to -75 mV (background current), suggesting the reversal potential of the DCB-inhibited current to be shifted by ca. 85 mV in the positive direction if Cai2+ rises following Ca2+ release. 5. The voltage dependence of the DCB-inhibited currents is highly compatible with the concept of Na+-Ca2+ exchange being the charge-carrying mechanism of the outward-rectifying background current. Ca2+ release from the SR alters the I-V curve of this current according to the shift of the thermodynamic driving force.