Communication between vascular smooth muscle cells (SMCs) allows control of arterial contraction and blood flow. The contractile state of the SMCs is regulated by cytosolic Ca2+ concentration and propagates as Ca2+ waves over a significant distance along the vessel. In this work, we studied an intercellular ultrafast Ca2+ wave observed in cultured A7r5 cell line and in primary cultured SMCs (pSMC) from mesenteric arteries obtained from male Wistar rats (250-350g) that were anesthetized with isoflurane (4%) and then decapitated in agreement with the Care of Animals (edited by the Swiss Academy of Medical Sciences and the Helvetic Society of Natural Sciences). Cells were aligned along networks obtained by photolithography technique. Using this microtechnique and a fast acquisition rate (330 Hz) allowed us to analyze fast intracellular Ca2+ fluorescence responses in different parts along the network after mechanical or KCl stimulation in one of the aligned cells. In addition, we have recorded and analyzed membrane potential variations in cells away from the mechanical stimulation site. Values are means ± S.E.M., compared by Student’s t-test on paired data. For both types of vascular SMCs, mechanical stimulation evoked an intercellular ultrafast Ca2+ wave with the same velocity (VpSMC=13.9±4.2mm/s, npSMC=10; VA7r5=16.3±3.9mm/s, nA7r5=16; p<0.01). Local KCl stimulation also induced an ultrafast Ca2+ wave that had the same magnitude for both SMCs (VpSMC=15.0±2.9mm/s, npSMC=7; VA7r5=14.5±2.7mm/s, nA7r5=9; p<0.01). The rate of increasing cytosolic Ca2+ along the network, decreased with distance from the stimulation site for both cases. Experiments performed in the presence of the gap junction uncoupler Palmitoleic acid (PA) (50µM) or in the presence of L-type voltage operated Ca2+ channel (VOCC) inhibitor Nifedipine (Nif)(10µM) suppressed the ultrafast Ca2+ wave propagation in all cases (npSMC,Nif=5; nA7r5,Nif=7; npSMC,PA=3; nA7r5,PA=5), inferring the crucial role of the electrical coupling through gap junctions and the importance of Ca2+ entry through the VOCCs for the ultrafast Ca2+ wave intercellular propagation. On the other hand, mechanical stimulation induced a membrane depolarization that propagated and decayed exponentially with distance. Both types of SMCs present different space constants (λpSMC=0.67mm, λA7r5=0.92mm). Our results suggest that in cultured vascular SMCs, an electrotonic spread of membrane depolarization drives the Ca2+ entry from the external media which can be modeled as an ultrafast Ca2+ wave. This ultrafast Ca2+ wave may triggers the Ca2+ release from intracellular stores that drives observed slower Ca2+ waves.