The endothelium lining the wall of resistance arteries and arterioles provides both chemical and electrical input to surrounding smooth muscle cells. Factors can be released and hyperpolarizing current can pass through myoendothelial gap junctions, when present. Many of the diffusible factors and indeed the hyperpolarization of endothelial and smooth muscle cells can occur secondary to increases in endothelial cell Ca²⁺, which can been seen as focal or propagating asynchronous Ca²⁺ waves within cells. We have recently shown that the projections of endothelial cells to smooth muscle cells form a distinct signalling microdomain, not all that dissimilar to synapses. The distance for diffusion of agents acting at smooth muscle receptors and proteins is shorter in this domain, and concomitantly, key proteins are expressed at high levels. Not only are factors and current able to stimulate local dilation, but current, and to a much lesser extent an intercellular Ca²⁺ signal, can pass longitudinally along the artery wall to stimulate dilatation upstream, termed conducted dilatation. It is thought that the diffusing intercellular Ca²⁺ signal is too slow to underlie the conducted dilatation. Nevertheless, increases in endothelial cell Ca²⁺ can stimulate both local and conducted dilatation. As an additional contribution by Ca²⁺ signalling to conducted dilatation, we have most recently shown that the frequency of focal, spontaneous Ca²⁺ events (puffs or pulsars) is increased following increases in membrane potential, and that as a consequence, this occurs at the upstream 'conducted' sites in cells not directly stimulated by the agonist. This process may help to amplify conducted dilatation responses, and occurs secondary to hyperpolarization but does not rely on an intercellular 'Ca²⁺ wave'. Overall the focal Ca²⁺ events and global changes in endothelial cells influence the diameter of arteries, and conducted dilatation serves to further reduce vascular resistance to potentially improve blood flow.