Hypokalaemic periodic paralysis (HypoPP) is an autosomal dominant muscle disease which has been linked to point mutations in the skeletal muscle L‐type calcium channel α ₁ subunit (α _1S ). Here, we have introduced one of the point mutations causing HypoPP (R528H) into cDNA of the rabbit α _1S . Expression of either the wild‐type α _1S or the mutant R528H α _1S (α ₁ S−R528H) subunit was obtained in mouse Ltk⁻ cell using a selectable expression vector. The α _1S−R528H subunit led to the expression of functional L‐type Ca²⁺ channels. Corresponding whole‐cell Ba²⁺ currents exhibit very slow activation and inactivation kinetics, typical for recombinant skeletal Ca²⁺ channel currents. Voltage‐dependent activation and inactivation properties were similar for α _1S ‐and α _{1S − R528H} , as well as their sensitivity to the dihydropyridine agonist Bay K 8644. Differences in α _1S ‐and α _1S−R528H ‐directed channels reside in the Ba²⁺ current density, which was significantly reduced 3.2 fold in cells expressing α _{1S − R528H} . It was concluded that the R528H mutation of α _1S results in minor differences in the electrophysiological properties but significantly reduces the whole‐cell Ca²⁺ channel current in its amplitude.