Inward rectifier potassium channels in the HL-1 cardiomyocyte-derived cell line.

HL-1 is a line of immortalized cells of cardiomyocyte origin that are a useful complement to native cardiomyocytes in studies of cardiac gene regulation. Several types of ion channel have been identified in these cells, but not the physiologically important inward rectifier K+ channels. Our aim was to identify and characterize inward rectifier K+ channels in HL-1 cells. External Ba2+ (100 µM) inhibited 44 ± 0.05% (mean ± s.e.m., n = 11) of inward current in whole-cell patch-clamp recordings. The reversal potential of the Ba2+-sensitive current shifted with external [K+] as expected for K+-selective channels. The slope conductance of the inward Ba2+-sensitive current increased with external [K+]. The apparent Kd for Ba2+ was voltage dependent, ranging from 15 µM at -150 mV to 148 µM at -75 mV in 120 mM external K+. This current was insensitive to 10 µM glybenclamide. A component of whole-cell current was sensitive to 150 µM 4,4′-diisothiocyanatostilbene-2,2′-disulfonic acid (DIDS), although it did not correspond to the Ba2+-sensitive component. The effect of external 1 mM Cs+ was similar to that of Ba2+. Polymerase chain reaction using HL-1 cDNA as template and primers specific for the cardiac inward rectifier Kir2.1 produced a fragment of the expected size that was confirmed to be Kir2.1 by DNA sequencing. In conclusion, HL-1 cells express a current that is characteristic of cardiac inward rectifier K+ channels, and express Kir2.1 mRNA. This cell line may have use as a system for studying inward rectifier gene regulation in a cardiomyocyte phenotype. J. Cell. Physiol. 225: 751-756, 2010. © 2010 Wiley-Liss, Inc. [ABSTRACT FROM AUTHOR]