Ventricular myocytes of the mouse ventricle were voltage clamped with a pat
ch-clamp technique in the whole-cell configuration. At depolarizing voltage
pulses, these myocytes develop a large voltage-dependent K+ outward curren
t. Application of the drug dibenzylamine (DBA) to the bath solution blocked
the voltage-dependent K+ current. The concentration/response relationship
for the peak current at +40 mV indicates a 1:1 binding of the drug to the r
eceptor with a concentration of half maximum effect of 43.1 mu mol/l. The b
lock did not require activation of the channels by depolarizing pulses. At
concentrations causing partial block (25 mu mol/l), the block was independe
nt of voltage. At the same concentration, DBA completely blocked the slow c
omponent of the recovery from inactivation (-80 mV) whereas steady-state in
activation was not altered. It is concluded that DBA is a novel blocker of
the voltage-dependent K+ current in mouse cardiac myocytes which preferenti
ally affects the current component generating the slow recovery from inacti
vation.