It has been increasingly recognized that dysfunction in endogenous pain regulatory systems may play a role in chronic pain. An important component of the endogenous pain regulatory process is the functional interaction between the cardiovascular and pain regulatory systems, which results in an inverse relationship between resting blood pressure (BP) and acute pain sensitivity. This inverse BP/pain sensitivity relationship is believed to reflect an adaptive homeostatic feedback loop that helps restore arousal levels in the presence of painful stimuli. The inverse BP/acute pain sensitivity relationship appears to be significantly altered (i.e., reversed) in chronic pain patients. It is proposed that these alterations reflect chronic pain-related dysfunction in normal pain regulatory processes. The overall objective of the proposed project is to identify underlying mechanisms that may account for these alterations in the BP/pain sensitivity relationship in chronic pain sufferers. In pain-free normotensives, baroreceptor-mediated mechanisms and alpha-2 adrenergic descending pain inhibitory pathways appear likely to contribute to expression of the inverse blood pain sensitivity relationship. Chronic pain-related decreases in baroreceptor sensitivity and/or impairments in adrenergic pain inhibitory pathways are hypothesized to mediate the altered blood pressure/pain sensitivity relationship in chronic pain sufferers. Chronic pain-related activation of descending pain facilatory pathways (central sensitization) that may interact with blood pressure regulation could also contribute to this altered BP/pain sensitivity relationship. Identifying the mechanisms responsible for chronic pain-related alterations in the BP/pain sensitivity relationship will contribute to improved understanding of the role of dysfunctional pain regulatory processes in chronic pain. Sixty chronic low back pain patients and 60 pain-free controls will participate in two laboratory sessions, once under alpha-2 adrenergic blockade with yohimbine and once under placebo. During each session, resting blood and spontaneous baroreceptor sensitivity will be determined, degree of central sensitization will be ascertained (reflected in temporal summation), and sensitivity to acute finger pressure, is chemic, and heat pain stimuli will be assessed. Data obtained from this protocol will be used to determine: 1) the extent to which alpha-2 adrenergic mechanisms contribute to the inverse BP/acute pain sensitivity relationship in pain-free normotensives,2) whether chronic pain-related impairments in alpha-2 adrenergio inhibitory pathways contribute to alterations in the blood pressure/acute pain sensitivity relationship across chronicpain/pain-free groups, 3) whether changes in baroreceptor sensitivity contribute to chronic pain-related alterations in the BP/pain sensitivity relationship, and 4) whether chronic activation of pain facilatory pathways contributes to alterations in the BP/pain sensitivity relationship. ? ?
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