ABSTRACT

At an embryonic stage, all cardiac cells, including the precursors of atrial and ventricular myocardium, are endowed with automatic activity. Development into mature atrial or ventricular phenotypes includes loss of automaticity; this is associated with the appearance of IK1,

1 whose properties are ideally suited to stabilize the membrane potential at a constant value, negative to the action potential excitation threshold. Thus, loss of automaticity, rather than its presence, might be viewed as a functional specialization. This view is the conceptual basis for the recent proposal to generate artificial “biological” pacemakers by suppressing transcription of IK1 channels in localized areas of the ventricles.2