(186) Relationship between central pain mechanisms and arterial blood pressure in pain free subjects

Abstract

Studies in humans suggest an interrelationship between blood pressure and pain regulation, where elevated resting blood pressure is associated with decreased pain sensitivity in pain free normotensives. However, it is still unclear whether: 1) this interrelationship involves peripheral and central arterial blood pressure, or 2) central pain mechanisms are involved. We classified 13 pain-free subjects (mean age = 47.46; SD= 7.32) as normotensive (n = 6) or prehypertensive (n = 7) using a systolic blood pressure >135 mm Hg as the cutoff. Heart rate (HR) and peripheral and central blood pressures were measured non-invasively before, during and after experimental pain procedures. Suprathreshold heat pain responses (SHPR) were generated with repeated thermal stimuli, and conditioned pain modulation (CPM) was assessed using SHPR as the experimental stimulus and cold pressor task (7 °C) as the conditioning stimulus. Repeated measures ANOVA showed significant increases (pre, during and post pain) in all measures of peripheral and central blood pressure; however, the time*group (normotensive vs prehypertensive) interaction was significant only for peripheral systolic pressure (F (2,18)=6.07, p=0.01) and central systolic pressure (F(2,18)=3.84, p=0.04). Significant positive associations were found between SHPR and arterial blood pressure (peripheral and central, p< 0.01) only in prehypertensive subjects. There was a significant positive association between the magnitude of CPM and HR difference in all subjects. These preliminary results imply that: 1) the acute response of peripheral and central systolic pressure differs between normotensive and prehypertensive individuals, where normotensives have a more pronounced response to pain induction, and 2) inhibitory (CPM) and facilitatory (SHPR) central pain mechanisms are related to different cardiovascular mechanisms in response to acute pain induction. Further analyses in a larger sample and in chronic pain patients will provide stronger evidence about the interrelationship between blood pressure and central pain mechanisms. Supported by Charlotte Zietlow Research Grant, Indiana State University.