Abstract
It is known that the amplitude of the outward current of the strong inward rectifier K+ current, IK1, in the atrium is smaller than that in the ventricle. However, the mechanism underlying the difference is not understood. Using the amphotericin B perforated-patch recordings, we found that the inward rectification of IK1 in the atrial cells of the guinea-pig heart was stronger than that in the ventricular cells. Further, the outward transients of IK1, which were elicited on repolarization in the ventricular cells, were hardly observed in the atrial cells. When the genes encoding the strong inward rectifier K+ channels Kir2.x, known to be expressed in the cardiac cells, were expressed in L cells, the inward currents of the Kir2.1 and Kir2.2 channels were similar to those of IK1, while those of the Kir2.3 channels were different with respect to their significantly slower activation and strong sensitivity to the external pH. When the outward currents of Kir2.1 and Kir2.2, known to be regulated by the blockage of the channel by cytoplasmic polyamines and Mg2+, were recorded from the inside-out patches in the co-presence of 1 mM Mg2+ and 5-10 μM spermine, marked transient currents were observed on repolarization. The amplitude of the transients became minimal when the concentrations of spermine and spermidine coexisting with Mg2+ were increased to a level higher than ~30 μM. Our results suggest that the difference in IK1 between the atrium and the ventricle is at least partly caused by higher concentrations of free polyamines in the atrial cells than in the ventricular cells. [Jpn J Physiol 54 Suppl:S99 (2004)]
