Muscular arteries are able to actively modify their diameter by modulating the tone of the smooth muscle cells located within the arterial wall. A small variation of lumen diameter has a large influence on blood flow as well as on arterial pressure. The cardiovascular system pressure is mainly regulated by the resistance arteries and arterioles. Most of these arteries show cyclic variations of their diameter. This phenomenon is known as vasomotion and is in no way linked to any other physiological cycle like heartbeat or respiratory cycles. This phenomenon can be observed as well in vivo as in vitro. The arterial diameter oscillations are attributed to the contractile activity of the smooth muscle cells which is directly linked to their intracellular calcium concentration. Although observed since years, the mechanisms underlying vasomotion remain not well understood. It is known that arterial vasomotion is modified by apparition of abnormalities in the contractile mechanisms of arteries linked to cardiovascular diseases like hypertension. A better understanding of this phenomenon could therefore contribute to better treatments or diagnosis of such diseases. This thesis is divided in two parts which have each the goal to clear up a definite aspect of arterial vasomotion. The experiments have been performed in vitro on resistance arteries: the rat mesenteric arteries. These arteries have been observed under confocal fluorescence microscope allowing to quantify the intracellular calcium concentration in smooth muscle cells. In the first part of this work, we investigate the role played by the endothelium on arterial vasomotion. So far, contradictory results have been related in the literature about the role of the endothelium in the onset and maintenance of vasomotion. Even the elementary question of knowing if vasomotion can arise without an intact endothelium is quite controversial. To understand how the endothelium may either abolish or promote vasomotion, we have stimulated rat mesenteric arterial strips with a vasoconstrictor: the phenylephrine. Our results show that the endothelium is not necessary for vasomotion. However, when the endothelium is removed the phenylephrine concentration needed to induce vasomotion is lower and the rhythmic contractions occur for a narrower range of phenylephrine concentrations. By selectively inhibiting the endothelium-derived relaxing products, we demonstrate that these substances may either induce or abolish vasomotion. On the one hand, when the strip is tonically contracted in a non-oscillating state, an endothelium-derived relaxation may induce vasomotion. On the other hand, if the strip displays vasomotion, a relaxation may induce a transition to a non-oscillating state with a small contraction. In conclusion, our findings clarify the role of the endothelium on vasomotion and reconcile the seemingly contradictory observations reported in the literature. In the second part of this thesis we are interested in a vasomotion property not studied until now which is the propagation of vasomotion along arterial segments. The aim of this study is first to characterize these contraction waves, then in a second part to define what are the mechanisms allowing this propagation. We have stimulated rat mesenteric arterial strips with phenylephrine to obtain vasomotion and observed that the contraction waves are linked to intercellular calcium waves. A velocity of about 100 µm/s was measured for the two kinds of waves and this velocity was independent of the presence of the endothelium on the strip. To investigate the calcium wave propagation mechanisms, we have elaborated a method allowing a phenylephrine stimulation of a small area of the strip. No calcium propagation could be induced by this local stimulation when the strip was in its resting state. However, if a low phenylephrine concentration was added on the whole strip, local phenylephrine stimulations induced calcium waves spreading over a finite distance of almost 400 µm. The calcium wave velocity induced by local stimulation was identical to the velocity observed during vasomotion. This suggests that the propagation mechanisms are similar in the two cases. Using inhibitors of gap junctions and of voltage operated calcium channels, we have shown that the intercellular calcium wave propagation depends on the propagation of the smooth muscle cells depolarization. Finally, the results allow to propose a model of the mechanisms underlying the propagation of intercellular calcium waves along arterial segments during vasomotion.