Communication between vascular smooth muscle cells (SMCs) allows control of their contraction and so regulation of blood flow. The contractile state of SMCs is regulated by cytosolic Ca 2+ concentration ([Ca 2+ ] i ) which propagates as Ca 2+ waves over a significant distance along the vessel. We have characterized an intercellular ultrafast Ca 2+ wave observed in cultured A7r5 cell line and in primary cultured SMCs (pSMCs) from rat mesenteric arteries. This wave, induced by local mechanical or local KCl stimulation, had a velocity around 15mm/s. Combining of precise alignment of cells with fast Ca 2+ imaging and intracellular membrane potential recording, allowed us to analyze rapid [Ca 2+ ] i dynamics and membrane potential events along the network of cells. The rate of [Ca 2+ ] i increase along the network decreased with distance from the stimulation site. Gap junctions or voltage-operated Ca 2+ channels (VOCCs) inhibition suppressed the ultrafast Ca 2+ wave. Mechanical stimulation induced a membrane depolarization that propagated and that decayed exponentially with distance. Our results demonstrate that an electrotonic spread of membrane depolarization drives a rapid Ca 2+ entry from the external medium through VOCCs, modeled as an ultrafast Ca 2+ wave. This wave may trigger and drive slower Ca 2+ waves observed ex vivo and in vivo.