1 The effects of a new alkaloid, ervatamine, on transmembrane currents of frog atrial fibres were studied by the double sucrose gap voltage clamp technique. 2 Ervatamine (2.8 x 10(-4) M) blocked the action potential without altering the resting membrane potential. 3 The alkaloid depressed the peak INa. The dissociation constant for the blocking effect of ervatamine on gNa fast was 2.35 X 10(-5) M with a one to one relationship between the drug molecule and the Na channel. Ervatamine did not alter the apparent equilibrium potential for Na, as well as the activation and inactivation parameters of gNa fast. This suggests that the alkaloid inhibitory effect on gNa can be attributed to a reduction in gNa. 4 Ervatamine prolonged the rate of reactivation of the Na system. It inhibited gNa in a frequency-dependent manner; this indicates that the alkaloid acts on open Na channels i.e. that the drug has to enter the channel or cross the membrane to produce the block. 5 Ervatamine inhibited Ina slow which occurs in Ca-free, tetrodotoxin-containing solutions and moderately decreased ICa which occurs in Na-free solutions. The drug increased the background K current (IK1) and did not alter the time-dependent K current (Ix1). 6 The present study shows that ervatamine is a good inhibitor of both fast and slow gNa. This drug also shares some common electrophysiological properties with antiarrhythmic drugs namely: the frequency-dependent inhibition of the fast gNa and the ability to slow the reactivation of the Na carrying system.