We tested the hypothesis that local and tight coupling between the Ca_v1.2 channels and RyRs is not required to initiate Ca²⁺ sparks in arterial vascular smooth muscle cells (VSMC). Cross-signalling between Ca_v1.2 channels and RyRs was studied using an approach based on Poisson statistical analysis of elementary calcium release events (ECRE). ECRE were recorded as Ca²⁺ sparks or STOCs in tibial VSMCs of smooth muscle-specific L-type Ca_v1.2 channel knockout (SMAKO) mice. Ca_v1.2 channel gene inactivation reduced Ca²⁺ spark frequency and amplitude by ~50% and ~80%, respectively. The first-latency histograms of sparks only slightly depended on the depolarization level and peaked at a relatively positive potential in wild-type VSMCs, i.e. ~+20 mV. Furthermore, average latencies between -30 mV and +50 mV occurred at ≥ 100 ms. Average latency of the first identified STOCs was similar and ≥ 100 ms in wild-type, nimodipine-treated and SMAKO VSMC and only slightly depended on the depolarization level. All-latency histograms in all three VSMC cell groups did not show a tendency to decline upon depolarization time. The observation that the first-latency and all-latency histograms have different waveforms implies that the release waveform is not determined by the time course of first event activation, with relatively fewer re-openings, as is the case in skeletal and cardiac muscle. Thus, Ca_v1.2 channels are important for frequency and amplitude modulation of VSMC Ca²⁺ sparks. However, local and tight coupling between the Ca_v1.2 channels and RyRs is not required to initiate Ca²⁺ sparks from single calcium release units in arterial VSMC.