RESUMO
The interaction of cardiovascular dynamics and pain perception is an important component of intrinsic pain regulation. In healthy subjects acute pain stimuli cause increased sympathetic arousal and increased mean arterial pressure. Arterial baroreceptors sense phasic blood pressure changes and relay the information to the lower brainstem via the dorsomedial nucleus tractus solitarius (dmNTS). Projections in the brainstem and also higher cortical areas result in elevation of blood pressure as part of the autonomic nervous system as well as modulation of sleep, anxiety and pain. In healthy subjects there is an inverse relationship between blood pressure and pain sensitivity but this relationship is impaired in chronic pain patients. Persistent stress, pain behavior and classical and operant conditioning mechanisms reduce baroreflex sensitivity (BRS) and dmNTS activity in a subgroup of patients. This leads to a decrease of autonomic regulatory function as well as reduced pain inhibition. Importantly, baroreflex function can be modulated by cognitive and affective processes. This article reviews the role of the baroreflex arc as a possible crucial factor in the development and maintenance of chronic pain. The importance of learning mechanisms is described. Mechanism-based individualized treatment approaches for patients with hypertensive stress reactivity are also critically discussed.
