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J Appl Physiol 99: 587-592, 2005. First published March 31, 2005; doi:10.1152/japplphysiol.00147.2005
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Selective {alpha}2-adrenergic properties of dexmedetomidine over clonidine in the human forearm

Shizue Masuki,1 Frank A. Dinenno,2 Michael J. Joyner,1 and John H. Eisenach1

1Department of Anesthesiology, Mayo Clinic, College of Medicine, Rochester, Minnesota; and 2Department of Health and Exercise Science, Colorado State University, Fort Collins, Colorado

Submitted 4 February 2005 ; accepted in final form 24 March 2005

We tested the hypothesis that dexmedetomidine (Dex) has greater {alpha}2- vs. {alpha}1 selectivity than clonidine and causes more {alpha}2-selective vasoconstriction in the human forearm. After local {beta}-adrenergic blockade with propranolol, forearm blood flow (plethysmography) responses to brachial artery administration of Dex, clonidine, and phenylephrine ({alpha}1-agonist) were determined in healthy young adults before and after {alpha}2-blockade with yohimbine (n = 10) or {alpha}1-blockade with prazosin (n = 9). Yohimbine had no effect on phenylephrine-mediated vasoconstriction but blunted Dex-mediated vasoconstriction (mean ± SE: –41 ± 5 vs. –11 ± 2%; before vs. after yohimbine) more than clonidine-mediated vasoconstriction (–39 ± 5 vs. –28 ± 4%; before vs. after yohimbine) (P < 0.02). Prazosin blunted phenylephrine-mediated vasoconstriction (–39 ± 4 vs. –8 ± 2%; before vs. after prazosin) but had similar effects on both Dex- (–30 ± 4 vs. –39 ± 6%; before vs. after prazosin) and clonidine-mediated vasoconstriction (–29 ± 3 vs. –41 ± 7%; before vs. after prazosin) (P > 0.7). Both Dex and clonidine reduced deep forearm venous norepinephrine concentrations to a similar extent (–59 ± 12 vs. –55 ± 10 pg/ml; Dex vs. clonidine, P > 0.6); this effect was abolished by yohimbine and blunted by prazosin. These results suggest that Dex causes more {alpha}2-selective vasoconstriction in the forearm than clonidine. The similar vasoconstrictor responses to both drugs after prazosin might be explained by the presynaptic effects on norepinephrine release.

forearm blood flow; sympathetic nervous system; vasoconstriction; resistance vessels


Address for reprint requests and other correspondence: J. H. Eisenach, Dept. of Anesthesiology, Mayo Clinic, 200 First St. SW, Rochester, MN 55905 (eisenach.john{at}mayo.edu)




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