Progression of cardiac potassium current modification after brief exposure to reactive oxygen

We reported previously that singlet oxygen (1O2), generated by illuminating the photosensitizer rose bengal (RB), suppressed the delayed rectifier potassium current (IK) in single frog atrial cells. Considering the brief lifetime of 1O2, one might expect IK modification to reach a steady-state soon after a brief exposure to RB-generated 1O2. Here we report that, contrary to expectations, tens of seconds can be required for IK to reach a new steady-state. We will use the term "progression" to refer to the component of current modification which occurs after cessation of illumination. To gain insight into the mechanism of progression, we investigated how its time course and magnitude were affected by (1) membrane potential during and following RB illumination, and (2) the level of IK activation during illumination. We found that conditions which favored the open state of the potassium channel also favored progression, increasing both its time course and magnitude. Illumination while IK was activated produced significant progression having a very slow time course (tens of seconds). By comparison, illumination when IK was not activated produced no progression: IK modification was completed during the 2 s illumination period. These findings suggest progression results from the kinetics of potassium channel state transitions rather than from a long-lived reactive intermediate produced during the initial 1O2 exposure.