This article reviews the basic physiology of the reflexogenic areas of the heart and the mechano- and baroreceptors that regulate cardiovascular and autonomic homeostasis, all of which contribute to our understanding of the pathogenesis of neurally mediated syncope. The mechanisms of neurally mediated syncope may involve excessive activation of ventricular receptors that trigger severe hypotension and bradycardia. Thus, neurally mediated syncope may be the clinical expression of the Bezold-Jarisch reflex, which occurs in situations of increased sympathetic activity, perhaps as a result of heightened cardiac receptor sensitivity. The arterial baroreceptors exert a ubiquitous influence on the heart and circulation, and serve primarily to buffer transient changes in arterial pressure by transmitting sensory information regarding their stretch to the central nervous system. This information, in conjunction with cardiac receptor input, elicits alterations in neural efferent output from sympathetic and parasympathetic fibers to provide subtle, continuous regulation of beat-to-beat cardiovascular hemodynamics to an array of physiologic and psychological stressors.