Characterization of chromanol 293B-induced block of the delayed-rectifier K+ current in heart-derived H9c2 cells.

The effects of chromanol 293B on ion currents in rat embryonic heart-derived H9c2 cells were investigated in this study. Chromanol 293B suppressed the amplitude of delayed rectified K+ current (I(K)) in a concentration-dependent manner. The IC50 value for chromanol 293B-induced inhibition of I(K) was 8 microM. The I(K) present in these cells, the electrical properties of which resembled those for the Kv2.1-related K+ current, was sensitive to inhibition by quinidine or dendrotoxin, yet not by pandinotoxin-Kalpha, E-4031 or apamin. Chromanol 293B reduced the activation time constant of I(K) and the effective gating charge of this channel. However, little or no modification in the steady-state inactivation of I(K) in response to long-lasting conditioning pulses could be demonstrated in the presence of chromanol 293B. These results clearly demonstrate that chromanol 293B can effectively interact with the K+ channel functionally expressed in H9c2 myoblasts. The chromanol 293B-induced inhibition of these channels could primarily be attributed to open channel block.