Electrophysiological and molecular characteristics of voltage‐dependent calcium (Ca2+) channels were studied using whole‐cell patch clamp, polymerase chain reaction and Western blotting in smooth muscle cells freshly isolated from dog basilar artery. Inward currents evoked by depolarizing steps from a holding potential of –50 or –90 mV in 10 mm barium consisted of low‐ (LVA) and high‐voltage activated (HVA) components. LVA current comprised more than half of total current in 24 (12%) of 203 cells and less than 10% of total current in 52 (26%) cells. The remaining cells (127 cells, 62%) had LVA currents between one tenth and one half of total current. LVA current was rapidly inactivating, slowly deactivating, inhibited by high doses of nimodipine and mibefradil (> 0.3 μm), not affected by ω‐agatoxin GVIA (γ100 nm), ω‐conotoxin IVA (1 μm) or SNX‐482 (200 nm) and probably carried by T‐type Ca2+ channels based on the presence of messenger ribonucleic acid (mRNA) and protein for Cav3.1 and Cav3.3α1 subunits of these channels. LVA currents exhibited window current with a maximum of 13% of the LVA current at –37.4 mV. HVA current was slowly inactivating and rapidly deactivating. It was inhibited by nimodipine (IC50= 0.018 μm), mibefradil (IC50= 0.39 μm) and ω‐conotoxin IV (1 μm). Smooth muscle cells also contained mRNA and protein for L‐ (Cav1.2 and Cav1.3), N‐ (Cav2.2) and T‐type (Cav3.1 and Cav3.3) α1 Ca2+ channel subunits. Confocal microscopy showed Cav1.2 and Cav1.3 (L‐type), Cav2.2 (N‐type) and Cav3.1 and Cav3.3 (T‐type) protein in smooth muscle cells. Relaxation of intact arteries under isometric tension in vitro to nimodipine (1 μm) and mibefradil (1 μm) but not to ω‐agatoxin GVIA (100 nm), ω‐conotoxin IVA (1 μm) or SNX‐482 (1 μm) confirmed the functional significance of L‐ and T‐type voltage‐dependent Ca2+ channel subtypes but not N‐type. These results show that dog basilar artery smooth muscle cells express functional voltage‐dependent Ca2+ channels of multiple types.