Blood pressure-related hypoalgesia: insights from heart-brain pathways

Abstract

Background: High blood pressure (BP) is characterized by reduced pain sensitivity, known as BP-related hypoalgesia. The cause of such phenomenon has not been clarified, yet existing studies point to a key role of the arterial baroreceptors. We studied the neural correlates of pain perception during discharge of baroreceptors, activated naturally at systole by phasic ejection of blood from the heart. Methods: After determining individual pain thresholds, normotensive participants underwent an event-related fMRI design in which unpredictable painful and non-painful electric shocks timed to occur either at systole or diastole were delivered. Participant also underwent a 1-week home BP monitoring. Findings: At behavioral level, mixed models showed the least pain perception when painful stimuli were administered at systole compared to diastole (p=0.03). When the group was divided into high and low systolic BP based on the median split, a main effect of BP status emerged with the high-BP group having overall lower pain perception (p=0.05). Neuroimaging data revealed a main effect of Stimulus in a) right calcarine cortex, extending ventrally to the cerebellum, b) right postcentral gyrus, extending anteriorly to the right precentral gyrus and encompassing the right supplementary motor area; c) right insula. For the effect of Cardiac phase, a cluster located in the right postcentral gyrus emerged. Discussion: Results support that the negative association between BP and pain perception is stronger during baroreceptor discharge. Given that BP-related hypoalgesia interferes with early detection of myocardial infarction in an “at risk groupâ€, the clarification of its basis has critical clinical implications.