Intercellular communication ensures a coordinated behaviour of vascular cells which is reflected by uniform diameter changes of arterioles over considerable distances. Conducted dilations can be elicited by local application of acetylcholine (ACh), bradykinin or adenosine. These substances hyperpolarize the cells, which is thought to be the signal that elicits a coordinated dilation. The locally initiated hyperpolarization spreads along the vessel through intercellular channels (gap junctions) composed of connexins (Cx). In vascular cells Cx40, Cx43, Cx37, and Cx45 are expressed, of which Cx40 is especially important because conducted dilations initiated by ACh or bradykinin are attenuated in Cx40-deficient animals. The function of Cx40 cannot be replaced by Cx45 expressed instead of Cx40 which suggests that specific Cx-properties are necessary to support conduction along the endothelium in which Cx40 is abundantly expressed. In contrast to ACh and bradykinin, conducted dilations initiated by adenosine are not attenuated in Cx40-deficient mice suggesting a distinct pathway possibly the smooth muscle cell layer. This is further supported by divergent properties of conducted dilations initiated by adenosine or ACh. Our data thus indicate that distinct pathways composed of different connexins are provided in arterioles to promote a coordinated diameter changes along the vessel length.