Ca²⁺ sparklets are local elevations in intracellular Ca²⁺ produced by the opening of a single or a cluster of L-type Ca²⁺ channels. In arterial myocytes, Ca²⁺ sparklets regulate local and global intracellular Ca²⁺. At present, the molecular identity of the L-type Ca²⁺ channels underlying Ca²⁺ sparklets in these cells is undetermined. Here, we tested the hypotheses that Cav1.3 channels can produce Ca²⁺ sparklets and that Cav1.2 and/or Cav1.3 channels are responsible for Ca²⁺ sparklets in mouse arterial myocytes. First, we investigated the functional properties of single Cav1.3 channels in tsA-201 cells. With 110 mM Ba²⁺ as the charge carrier, Cav1.3 channels had a conductance of 20 pS. This value is similar to that of Cav1.2 and native L-type Ca²⁺ channels. As previously shown for Cav1.2 channels, Cav1.3 channels can operate in two gating modes characterized by short and long open times. Expressed Cav1.3 channels also produced Ca²⁺ sparklets. Cav1.3 sparklets had properties similar to those produced by Cav1.2 and native L-type channels including quantal amplitude, dihydropyridine sensitivity, bimodal gating, and dual event duration times. However, the voltage dependencies of conductance and steady-state inactivation of the Ca²⁺ current (I_Ca) in arterial myocytes were similar to those recorded from cells expressing Cav1.2, but not Cav1.3 channels. Furthermore, nifedipine (10 µM) eliminated Ca²⁺ sparklets in wild type myocytes, but not in myocytes expressing dihydropyridine-insensitive Cav1.2 channels. Accordingly, Cav1.3 transcript and protein were not detected in isolated arterial myocytes. We conclude that although Cav1.3 channels can produce Ca²⁺ sparklets, Cav1.2 channels underlie I_Ca, Ca²⁺ sparklets, and hence dihydropyridine-sensitive Ca²⁺ influx in mouse arterial myocytes.