Non‐technical summary  Appropriate regulation of ion channel expression is critical for the maintenance of both electrical stability and normal contractile function in the heart. A classic way to study the robustness of biological systems is to examine the effects of changes in gene dosage. We have studied how the heart responds to changes in the L‐type calcium channel gene dosage. Homozygous Cav1.2 knockout in the adult heart is lethal, without compensatory responses in expression of other calcium channel genes. Following heterozygous knockout, Cav1.2 mRNA levels are not buffered, Cav1.2 membrane protein levels are partly buffered and L‐type calcium current expression is relatively well buffered. These data are consistent with a passive model of Cav1.2 biosynthesis that includes saturated steps, which act to buffer Cav1.2 protein and L‐type calcium current expression. The results suggest that there is little or no homeostatic regulation of calcium current expression in either heterozygous or homozygous knockout mice.