The relationship between resting blood pressure and acute pain sensitivity: effects of chronic pain and alpha-2 adrenergic blockade

Abstract

This study tested for alpha-2 adrenergic mediation of the inverse relationship between resting blood pressure and acute pain sensitivity in healthy individuals. It also replicated limited prior work suggesting this inverse blood pressure/pain association is altered in chronic pain, and provided the first test of whether chronic pain-related changes in alpha-2 adrenergic function contribute to these alterations. Resting blood pressure was assessed in 32 healthy controls and 24 chronic low back pain participants prior to receiving placebo or an intravenous alpha-2 adrenergic receptor antagonist (yohimbine hydrochloride, 0.4 mg/kg) in a randomized crossover design. Participants experienced three acute pain tasks during both sessions. A significant Systolic Blood Pressure x Participant Type x Drug interaction on finger pressure McGill Pain Questionnaire-Sensory ratings (P < .05) reflected significant hyperalgesic effects of yohimbine in chronic pain participants with lower systolic blood pressures (P < .05) but not those with higher systolic pressures, and no significant effects of yohimbine in controls regardless of blood pressure level. A Drug x Systolic Blood Pressure interaction on finger pressure visual analog scale unpleasantness indicated the inverse blood pressure/pain association was significantly stronger under yohimbine relative to placebo (P < .05). Significant Participant Type x Systolic Blood Pressure interactions (P's < .05) were noted for finger pressure visual analog scale pain intensity and unpleasantness, ischemic pain threshold, and heat pain threshold, reflecting absence or reversal of inverse blood pressure/pain associations in chronic pain participants. Results suggest that blood pressure-related hypoalgesia can occur even when alpha-2 adrenergic systems are blocked. The possibility of upregulated alpha-2 adrenergic inhibitory function in chronic pain patients with lower blood pressure warrants further evaluation.

Chronic pain, body mass index and cardiovascular disease risk factors: tests of moderation, unique and shared relationships in the Study of Women’s Health Across the Nation (SWAN)

“…If chronic pain is conceptualized more broadly as a chronic physiological stressor, one possibility is that chronic stress-related activations of the sympathoadrenomedullary and hypothalamo-pituary-adrenocortical axes may contribute to increased incidence of metabolic syndrome (Nieuwenhuizen & Rutters, 2008; Rosmond, 2005). Other studies provide evidence for chronic pain-related reductions in baroreflex sensitivity indicating altered autonomic function (Chung et al, 2008; Furlan et al, 2005; Reyes Del Paso, Garrido, Pulgar, Martín-Vázquez, Duschek, 2010; Spaziani, 2008), absence of natural analgesia typically associated with BP elevations (Bruehl, Chung, Diedrich, Diedrich, Robertson, 2008; Olsen et al, in press; Bruehl, Chung, & Chont, 2010; Bruehl, Chung, Ward, Johnson, & McCubbin, 2002), and possible alterations in neurotransmitter function including opioid (Bruehl & Chung, 2004; Bruehl, McCubbin, & Harden, 1999; Spaziani et al, 2008) and alpha-2 adrenergic (Chung et al, 2008) systems. These findings suggest that chronic pain is associated with changes in both the central and peripheral nervous systems that could provide alternative pathways for elevated CVD risk.…”

Is Resolution of Chronic Pain Associated With Changes in Blood Pressure-related Hypoalgesia?

“…The BP variables used in the analyses below reflected the mean of these four resting BP readings. Because previous studies have often shown little association between diastolic BP (DBP) and evoked pain measures [1,2,10,11,19,25], the results below focus on the influences of systolic BP (SBP). As expected, analyses for DBP paralleling those described below for SBP revealed no significant main or interaction effects involving DBP (all p > .23; results not detailed).…”

“…These BP increases trigger baroreceptors that activate descending pain inhibitory pathways from the brain to produce analgesic effects and restore cardiovascular homeostasis [9]. Although mechanisms underlying this BP-related hypoalgesia in humans are not fully understood, there is evidence that both endogenous opioid and α 2 -adrenergic pathways may be involved [10][11][12][13].…”

Preoperative Pain, Symptoms, and Psychological Factors related to Higher Acute Pain Trajectories during Hospitalization for Total Knee Arthroplasty

“…Higher levels of C-reactive protein and obesity are associated with higher levels of pain in patients with OA but the impact on postoperative pain is not known [22]. Lower resting blood pressure levels are been associated with lower acute pain thresholds [23]. …”