L-type voltage gated calcium channels are responsible for calcium entry into vascular smooth muscle cells (VSMC), which plays a role in excitation-contraction coupling, cell migration and growth. We previously reported that growth arrest by serum deprivation was associated with increased functional importance of L-type calcium channels in human VSMC [1]. In this study we examined if growth arrest was associated with a change in expression of L-type calcium channel subunits, α1, α2δ-1 and β3. Human VSMC were grown from explant cultures of saphenous vein and confluent cells at passage 3 were growth arrested by serum deprivation for up to 7 days. mRNA expression was measured by real-time PCR with SYBR Green and normalized to 2 reference genes, 18SrRNA and RPLP0. Protein expression was measured by SDS-PAGE and Western blotting using specific antibodies to the different L-type calcium channel subunits, and normalized to β-actin. Data are means ± SEM of 3 – 4 separate experiments. Serum deprivation for 5 days significantly increased α1 subunit mRNA expression (97±29% increase; p = 0.008). No significant difference was observed in α2δ-1 mRNA (18±10% decrease; p = 0.2), while a small increase was noted in the mRNA for the β3 subunit in growth arrested cells (44±9% increase; p = 0.007). There was also a time-dependent increase in levels of α1 and α2δ-1 protein following serum deprivation for up to 7 days (Table 1). The maximum increases in α1 and α2δ-1 were 40% and 34% respectively at day 7 of growth arrest. There was no significant change in β3 protein expression. The increase in functional L-type calcium channels following growth arrest of human VSMC is probably largely due to an increased expression of α1 subunit, although increased levels of α2δ-1 protein may also play a role. Changes in L-type calcium channel subunit expression during phenotypic modulation of VSMC may account for the failure of calcium channel antagonists to inhibit atherosclerosis in some studies in vivo.