Abstract
Recent studies have shown the presence of a 4-aminopyridine (4-AP) sensitive, ultrarapid delayed rectifier K+ current (IK,ur) in adult human atria, but an apparent absence of this current in adult human ventricles. The present experiment was designed to investigate the postnatal changes of IK,ur in rat ventricular myocytes. The presence of IK,ur was evaluated with the use of a low concentration of 4-AP (50 micro;M). In 3-day-old newborns, the channel activity of rapidly activating outward current was predominantly the transient outward current (Ito). IK,ur could be recorded in a small number of 3-day-old cells lacking Ito (16%). In 10-day-old and adult rat ventricular myocytes, almost all cells expressed Ito and its current density increased significantly with age. The fraction of cells expressing IK,ur dramatically decreased with age and no IK,ur-like component could be detected in the adult cells. These findings first demonstrate that the expression of IK,ur is regulated developmentally in mammalian ventricular myocytes.
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