Major lines of evidence suggest that classical (emotional and orthostatic) vasovagal syncope (VVS) is not a disease, but rather a manifestation of a non-pathological trait. It is, therefore, reasonable to investigate the possible factors that may explain its origin and evolution. We reviewed the data available in the literature on the vasovagal reaction in humans and animals in order to identify possible similarities that might provide insight into the evolution of VVS. We found two processes which appear relevant to the investigation of VVS evolution: fear and threat bradycardia in animals, and the vasovagal reflex during hemorrhagic shock in humans and animals. We suggest that VVS in humans involves physiological mechanisms similar to those found in other vertebrates, and that this may indicate a common evolutionary root. The available data seem to suggest that VVS evolved as an advantageous response to inescapable predators or to stressful and possibly dangerous heart conditions. The inhibition of the sympathetic system, together with activation of the vagal system, characterizes VVS. The consequent slowing of the heart rate induced by VVS may constitute a beneficial break of the cardiac pump, thereby reducing myocardial oxygen consumption. We suggest that classical VVS did not evolve recently in the modern human lineage; rather, it should be regarded as a selected response, which probably evolved in the ancient past as a "defense mechanism" of the organism within some ancestral group(s) of vertebrates.