EFFECTS OF NALOXONE ON HEMODYNAMIC AND SYMPATHETIC-NERVE RESPONSES TOPAIN IN NORMOTENSIVE VS. BORDERLINE HYPERTENSIVE MEN

Citation
Hp. Schobel et al., EFFECTS OF NALOXONE ON HEMODYNAMIC AND SYMPATHETIC-NERVE RESPONSES TOPAIN IN NORMOTENSIVE VS. BORDERLINE HYPERTENSIVE MEN, Journal of the autonomic nervous system, 69(1), 1998, pp. 49-55
Citations number
26
Categorie Soggetti
Neurosciences
ISSN journal
01651838
Volume
69
Issue
1
Year of publication
1998
Pages
49 - 55
Database
ISI
SICI code
0165-1838(1998)69:1<49:EONOHA>2.0.ZU;2-P
Abstract
Pain sensitivity decreases with increasing resting blood pressure. Thi s blood pressure-pain interaction may be mediated by endogenous opioid s which have been shown to affect both blood pressure and nociception. To test this hypothesis, we measured mean arterial blood pressure (MA P), central venous pressure (CVP), heart rate (HR), muscle sympathetic nerve activity (MSNA), serum catecholamines, and individual pain rati ng scales during 2 min periods of noxious mechanostimulation (skin fol d pinching) in nine young (26 +/- 2 year), male normotensive (NT) subj ects and in 12 age and weight matched males with borderline hypertensi on (BHT). Measurements were performed before and after the i.v. admini stration of naloxone (0.15 mg/kg) and placebo in a randomized double-b lind cross-over trial. In the pre-naloxone trials, pain led to similar changes in MAP, CVP, MSNA and plasma catecholamines in the two groups except for a higher increase in HR in the BHT group as compared to th e NT group (3 +/- 1 vs. 1 +/- 1 bpm; P < 0.005). Opioid blockade with naloxone increased MSNA responses to pain in the NT group (from 5 +/- 1 to 9 +/- 1 bursts/min, and, from 100 +/- 23 to 204 +/- 36 units/min, respectively; P < 0.05) but did not significantly affect the MSNA res ponse to pain in the BHT group. Pain induced responses of MAP, CVP, an d catecholamines were not altered by naloxone in either group. Overall , there was a highly significant inverse correlation between pain perc eption and resting blood pressure which was not significantly affected by naloxone. The BHT subjects exhibited a lower pain perception compa red to the NT subjects (P < 0.005). Naloxone increased pain rating in the NT group (from 194 +/- 9 to 218 +/- 13; P < 0.005) but not in the borderline hypertensive group (160 +/- 8 vs. 168 +/- 10; P = 0.36). Ex cept for a decreased HR response in the BHT group, placebo had no effe ct on the responses to pain. Our data do not indicate a major role of the endogenous opioid system for the blood pressure-pain interaction i n man. Endogenous opioids affect pain perception and sympathetic nerve activity responses to pain in normotensive men but their activity see ms to be attenuated in borderline hypertensive subjects. Therefore, th e lower pain sensitivity in human essential hypertension is probably m ediated by non-opioid mechanisms. (C) 1998 Elsevier Science B.V. All r ights reserved.