Communication between vascular smooth muscle cells (SMCs) allows control of their contraction and so regulation of blood flow. The contractile state of SMCs is controled by cytosolic Ca2+ concentration ([Ca2+]i) which propagates as Ca2+ waves over a significant distance along the vessel. In the first part, we have characterized an intercellular ultrafast Ca2+ 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 on a micro-fabricated substrate with fast Ca2+ imaging and intracellular membrane potential recording, allowed us to analyze rapid [Ca2+]i dynamics and membrane potential events along the network of cells. The rate of [Ca2+]i increase along the network decreased with distance from the stimulation site. Gap junctions or voltage-operated Ca2+ channels (VOCCs) inhibition suppressed the ultrafast Ca2+ wave. The second part is focused on the electrophysiology aspects of the mechanically-induced membrane depolarization. Mechanical stimulation induced a membrane depolarization that propagated and that decayed exponentially with distance. The spreading velocity of the membrane depolarization had a similar magnitude than the velocity of the ultrafast Ca2+ wave. In the last part, we tested the hypothesis that the ultrafast Ca2+ wave results from cell membrane depolarization propagation with the implementation of a mathematical model. The theoretical model reproduced qualitatively and quantitatively the main experimental findings that supported the conclusions of this thesis. Together, these results demonstrate that an electrotonic spread of the cell membrane depolarization drives a rapid Ca2+ entry from the external medium through VOCCs, modeled as an ultrafast Ca2+ wave. This wave may trigger and drive slower Ca2+ waves observed ex vivo and in vivo.