Calcitonin gene-related peptide, the main transmitter released from capsaicin-sensitive sensory-motor fibers, has positive inotropic and chronotropic effects on the heart and causes vasodilatation in the coronary arteries and elsewhere in the peripheral vasculature. We review some aspects of the cardiovascular actions induced by exogenous calcitonin gene-related peptide and by release of the peptide following activation of capsaicin-sensitive nerves. The efferent function of cardiac sensory-motor neurones is modulated by a number of endogenous substances of physiopathological interest, including opioid peptides, norepinephrine and adenosine. The receptors involved in the prejunctional regulation due to these substances have been characterized. Studies on the mesenteric bed of the rat have shown that, at least in such a resistance vascular bed, the relaxing effect of calcitonin gene-related peptide is mediated by a direct mechanism independent of endothelium-derived nitric oxide release. In cultured human endothelial cells from the umbilical cord vein, calcitonin gene-related peptide, at nM concentrations, stimulates cell growth in a dose-dependent manner. The possible implications of calcitonin gene-related peptide in the physio-pathological regulation of the cardiovascular system and in the trophism of vascular tissues are discussed.