Hypoalgesia associated with elevated resting blood pressure: evidence for endogenous opioid involvement

Bruehl, Stephen; Burns, John W.; Chung, Ok Yung; Magid, Edward B.; Chont, Melissa; Gilliam, Wesley P; Matsuura, J.; Somar, Kristin; Goodlad, James K.; Stone, Kevin H.; Cairl, Heather

doi:10.1007/s10865-009-9241-4

Cited by 32 publications

(23 citation statements)

References 53 publications

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“…This interpretation is weakened by the lack of direct correspondence between BE levels in plasma and the central nervous system 24,25 . Regarding possible gender moderation observed for one morphine effect outcome, presence of opioid-related effects specific to men are consistent with a few prior studies 50,55 .…”

Section: Discussionsupporting

confidence: 90%

Do Resting Plasma β-Endorphin Levels Predict Responses to Opioid Analgesics?

Bruehl

Burns²,

Gupta³

et al. 2017

The Clinical Journal of Pain

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Objectives Clinically-feasible predictors of opioid analgesic responses for use in precision pain medicine protocols are needed. This study evaluated whether resting plasma beta-endorphin (BE) levels predicted responses to an opioid analgesic, and whether chronic pain status or gender moderated these effects. Methods Participants included 73 individuals with chronic low back pain (CLBP) and 88 healthy controls, all using no daily opioid analgesics. Participants attended two identical laboratory sessions during which they received either intravenous morphine (0.08 mg/kg) or saline placebo, with blood samples obtained before drug administration to assay resting plasma BE levels. Once peak drug activity was achieved in each session, participants engaged in an ischemic forearm pain task (ISC) and a heat pain task. Morphine analgesic effects were derived reflecting the difference in pain outcomes between placebo and morphine conditions. Results In hierarchical regressions, significant Type (CLBP vs. Control) X BE interactions (p’s<.05) were noted for morphine effects on ISC tolerance, ISC intra-task pain ratings, and thermal VAS unpleasantness ratings. These interactions derived primarily from associations between higher BE levels and smaller morphine effects restricted to the CLBP subgroup. All other BE-related effects, including gender interactions, for predicting morphine analgesia failed to reach statistical significance. Discussion BE was a predictor of morphine analgesia for only 3 out of 9 outcomes examined, with these effects moderated by chronic pain status but not gender. On the whole, results do not suggest that resting plasma BE levels are likely to be a clinically useful predictor of opioid analgesic responses.

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Section: Discussionsupporting

confidence: 90%

Do Resting Plasma β-Endorphin Levels Predict Responses to Opioid Analgesics?

Bruehl

Burns²,

Gupta³

et al. 2017

The Clinical Journal of Pain

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“…Although hypertension-induced hypoalgesia is the most commonly described association of BP with pain threshold (Ghione, 1996), a negative correlation between the magnitudes of pain sensitivity and BP values has also been shown in normotensive individuals (Bruehl et al, 1992(Bruehl et al, , 2010Ditto et al, 1998). Therefore, although the BP increase induced by antisense vector was moderate (12% in SBP and 11% MAP), it is possible that the nociceptive effects observed in the present study are secondary to cardiovascular variations.…”

Section: Cardiovascular and Pain Effects Elicited By Nmda Manipulatiomentioning

confidence: 50%

Decrease in the expression of N‐methyl‐D‐aspartate receptors in the nucleus tractus solitarii induces antinociception and increases blood pressure

Marques-Lopes

Martins

Pinho

et al. 2011

J of Neuroscience Research

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N-methyl-D-aspartate receptors (NMDAR) have a role in cardiovascular control at the nucleus tractus solitarii (NTS), eliciting increases or decreases in blood pressure (BP), depending on the area injected with the agonists. In spite of the association between cardiovascular control and pain modulation, the effects of manipulating NMDAR in pain responses have never been evaluated. In this study, we decreased the expression of NMDAR in the NTS using gene transfer to target receptor subunits and evaluate long-term effects. Seven days after the injection of lentiviral vectors containing the NR1a subunit cDNA of NMDAR, in antisense orientation, into the intermediate NTS of Wistar rats, BP was measured, and the formalin test of nociception was performed. The antisense vector induced a decrease of NR1 expression in the NTS and elicited BP rises and hypoalgesia. Antisense vectors inhibited formalin-evoked c-Fos expression in the spinal cord, indicating decreased nociceptive activity of spinal neurons. Using a time-course approach, we verified that the onset of both the increases in BP and the hypoalgesia was at 4 days after vector injection into the NTS. The injection of NMDA into the NTS reversed the effects of antisense vectors in pain behavioral responses and spinal neuronal activation and decreased BP and heart rate. The present study shows that the NR1 subunit of the NMDAR at the NTS is critical in the regulation of tonic cardiovascular and nociceptive control and shows an involvement of the nucleus in the modulation of sustained pain.

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“…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).…”

Section: Methodsmentioning

confidence: 99%

“…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].…”

Section: Introductionmentioning

confidence: 99%

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

Coba

Bruehl

Garber

et al. 2018

Annals of Behavioral Medicine

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Background In healthy individuals, elevated resting blood pressure (BP) is associated with reduced pain responsiveness and lower temporal summation. Prior work indicates that this BP-related hypoalgesia is reduced in individuals with chronic pain. Purpose This study evaluated whether resolution of chronic pain was associated with greater BP-related hypoalgesia compared to nonresolution. Methods From a prospective sample of adolescents and young adults diagnosed with chronic functional abdominal pain an average of 9 years earlier, 99 individuals in whom the condition had resolved and 51 individuals with ongoing abdominal pain were studied. Resting systolic BP was assessed, followed by evaluation of thermal pain threshold and tolerance, and assessment of temporal summation to thermal pain stimuli. Results Higher resting systolic BP was significantly associated with higher pain threshold and tolerance, and lower temporal summation only in the group with resolved functional abdominal pain (p < .05). Hierarchical regressions revealed that interactions between BP and resolution of chronic pain were significant only for pain tolerance (p < .05). Analyses by sex indicated that interactions between BP and resolution status were significant for the temporal summation outcome in males but not in females.Conclusions Results suggest that BP-related hypoalgesic mechanisms may be more effective in individuals in whom chronic pain has resolved compared to those with ongoing chronic pain. Findings hint at sex differences in the extent to which resolution of chronic pain is associated with BP-related hypoalgesia. Whether greater BP-related hypoalgesia is a consequence of, or alternatively a contributor to, resolution of chronic pain warrants further investigation.

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Hypoalgesia associated with elevated resting blood pressure: evidence for endogenous opioid involvement

Cited by 32 publications

References 53 publications

Do Resting Plasma β-Endorphin Levels Predict Responses to Opioid Analgesics?

Do Resting Plasma β-Endorphin Levels Predict Responses to Opioid Analgesics?

Decrease in the expression of N‐methyl‐D‐aspartate receptors in the nucleus tractus solitarii induces antinociception and increases blood pressure

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

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