Abstract
The effects of a bufadienolide isolated from toad venom, arenobufagin, a potent Na +/K + pump inhibitor, were studied in single guinea-pig ventricular cells in the whole-cell patch-clamp configuration. Arenobufagin (50 μM) applied extracellularly decreased the amplitude of the delayed rectifier K + current ( I dK) by 30% without affecting the gating kinetics. The L-type Ca 2+ current was also depressed, but to a lesser extent. The inward rectifier K + current was hardly affected. Ouabain and the internal dialysis of cells with the solution containing 20 mM Na + depressed I dK in a similar way as arenobufagin. On the other hand, arenobufagin also depressed I dK when the Na +/K + pump was already inhibited in the K +-free Tyrode solution. Therefore, both a direct effect on the channel and an indirect effect through the inhibition of the Na +/K + pump may be involved in the depression of I dK by arenobufagin.
Published Version
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