Involvement of various areas of the body surface in heat emission response to warming is characterized by a certain succession. The first response preceding the deep body temperature rise is dilation of ear skin vessels. Then, an increase in deep body temperature is counterbalanced by vascular reaction in the tail region, which plays the leading role in up-regulation of heat emission. Calcium ions accelerate the vascular response to warming in both regions, although they produce no effect on the maximum level of heat emission. Our findings confirm the involvement of Ca(2+)-dependent mechanisms in activation of the processes aimed at stabilization of body temperature in warm-blooded animals. The role of heat-sensitive TRPV1 ion channels determining modality of the temperature signal and direction of effector reactions is discussed.