CHARACTERIZATION OF BETA SUBUNIT MODULATION OF A RABBIT CARDIAC L-TYPE CA-2+ CHANNEL ALPHA-1 SUBUNIT AS EXPRESSED IN MOUSE L-CELLS

Functional properties of a rabbit cardiac alpha1 Ca2+ channel subunit (CARDalpha1) were investigated using the patch-clamp technique in mouse L cells, a recipient cell line which is devoid of any Ca2+ channel subunits. Cell lines resulting from stable transfection of the CARDalpha1 subunit as well as in coexpression with a beta subunit (CARDalpha1beta) derived from skeletal muscle (SKMbeta) were characterized. The results show that while the CARDalpha1-Ca2+ channel activity is negligible, the Ba2+ current density is dramatically increased in the presence of beta subunit (approximately 20-fold). CARDalpha1- and CARDalpha1beta-Ba2+ currents were both sensitive to the 1,4-dihydropyridine (DHP) agonist, Bay K 8644 (5- to 8-fold increase). Activation kinetics of CARDalpha1- and CARDalpha1beta-Ba2+ currents were comparable. The inactivation time-course was faster (3- to 4-fold) for CARDalpha1beta-Ba2+ currents. We conclude that the main role of the beta subunit in heart is to modulate the L-type current density and present several lines of evidence that SKMalpha1 and CARDalpha1 are differentially regulated by the beta subunit.