Characterization of β subunit modulation of a rabbit cardiac L‐type Ca2+ channel α1 subunit as expressed in mouse L cells

Abstract
Functional properties of a rabbit cardiac α1 Ca2+ channel subunit (CARDα1) 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 CARDα1 subunit as well as in coexpression with a β subunit (cardα1β) derived from skeletal muscle (SKMβ) were characterized. The results show that while the CARDα1-Ca2+ channel activity is negligible, the Ba2+ current density is dramatically increased in the presence of β subunit (2̃0-fold). CARDα1- and CARDα1β-Ba2+ currents were both sensitive to the 1,4-dihydropyridine (DHP) agonist, Bay K 8644 (5- to 8-fold increase). Activation kinetics of CARDα1- and CARDα1β-Ba2+ currents were comparable. The inactivation time-course was faster (3- to 4-fold) for CARDα1β)-Ba2+ currents. We conclude that the main role of the β subunit in heart is to modulate the L-type current density and present several lines of evidence that SKMα1 and CARDα1 are differentially regulated by the β subunit.