Potassium channels and the repolarization of cardiac cells

What is the contribution of a particular potassium current to the repolarization of cardiac myocytes? The traditional answer to this question requires clamping the cells with step voltages, finding models that describe how individual currents depend on voltage and time, driving these models with action potentials to calculate the action currents, and evaluating the contribution of each pathway to repolarization from the action currents. Another method is to measure the action currents directly from beating cells. We isolated potassium channels in cell-attached patches and averaged the current over many beats. The average channel current, mean value of i(t), is a miniature version of the action current through corresponding channels in the membrane outside the patch. The time integral of this current, scaled by channel density, N, and membrane capacity, C, is the contribution of that particular pathway to the action potential: Vi(t) = -Ni integral of to mean value of i(u) du/C Using this procedure, we have found that the delayed rectifier, IK, turns on virtually without delay following the upstroke of the action potential and gradually declines during the plateau and repolarization phases, having nearly the shape of the action potential itself. The inward rectifier, IKl, may conduct little current during the plateau and is under the control of internal Ca. The traditional method of measuring action currents from step voltage-clamp records gives qualitatively similar results. Differences may arise because factors other than voltage modulate potassium currents in beating cells.