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Opioid Analgesia in Persons at Risk for Hypertension

McCubbin, James A. PhD; Helfer, Suzanne G. PhD; Switzer, Fred S. III PhD; Galloway, Cynthia RN; Griffith, William V. MD

doi: 10.1097/01.psy.0000195742.24850.79
Original Articles

Objective: Acute pain sensitivity is reduced in clinical hypertension, but the precise relationship between pain perception and altered blood pressure control is not well-characterized. A negative correlation between resting blood pressure and pain sensitivity is observed throughout the normotensive range, suggesting links between basic mechanisms of blood pressure control and pain regulation. The opioid peptides are important endogenous analgesic mechanisms, but their role in the hypoalgesia of blood pressure elevations has not been well-established. The current study sought to examine the effects of endogenous opioids on blood pressure-associated hypoalgesia in young adults at risk for hypertension development.

Methods: The effects of the opioid receptor antagonist, naltrexone, on cold pressor pain sensitivity were assessed in young adult men (n = 49) and women (n = 76) with mildly elevated casual blood pressure.

Results: Results indicate interactions between hypertension risk and the effects of opioid blockade on pain sensitivity.

Conclusions: These findings suggest exaggerated opioid analgesia in persons at enhanced risk for hypertension and point to important links between altered neuropeptide regulation of pain and altered blood pressure control mechanisms in the early stages of hypertension.

HR = heart rate; SBP = systolic blood pressure; DBP = diastolic blood pressure; MAP = mean arterial pressure; HPA = hypothalamic pituitary adrenocortical; CRF = corticotropin-releasing factor.

From Clemson University (J.A.M., F.S.S., C.G., W.V.G.), Clemson, SC; and Adrian College, Adrian, MI (S.G.H.).

Address correspondence and reprint requests to James A. McCubbin, PhD, Department of Psychology, Clemson University, 418 Brackett Hall, Clemson, SC 29634-1355. E-mail:

Received for publication November 15, 2004; revision received June 24, 2005.

This research was supported in part by NIH HL32738 to Dr. McCubbin and HL10227 to Dr. Helfer.

Copyright © 2006 by American Psychosomatic Society
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