Identification and characteristics of delayed rectifier K+ current in fetal mouse ventricular myocytes

Although the genetics of mammalian cardiac K+-channels have been most-intensively investigated in mice, there are limited data available from the electrophysiological studies of the K+ currents in native mouse cardiac myocytes, especially in fetal mouse heart. The present study utilized whole cell patch-clamp techniques to assess the delayed rectifier K+ current (I-K) in fetal (18th day of gestation) mouse ventricular myocytes. I-K in fetal mouse ventricular myocytes activated rapidly, displayed a negative slope conductance of the current-voltage relationships at test potentials >0 mV, satisfied the envelope of I-K-tail test-for a single component, and was very sensitive to dofetilide. These characteristics confirm that this current is the rapidly activating component of I-K known as I-K,I-r. In addition, dofetilide dramatically prolonged action potential duration in single ventricular myocytes as well as in ventricular myocardium, suggesting that I-K,I-r plays a dominant role in action potential repolarization in fetal mouse heart. From these data we can conclude that fetal mouse cardiac myocytes express I-K,I-r, which functions as a dominant repolarizing K+ current.