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2-adrenergic properties of dexmedetomidine over clonidine in the human forearm
1 Department of Anesthesiology, Mayo Clinic and Foundation, Rochester, MN, USA
2 Department of Health and Exercise Science, Colorado State University, Fort Collins, CO, USA
* To whom correspondence should be addressed. E-mail: Eisenach.John{at}mayo.edu.
We tested the hypothesis that dexmedetomidine (Dex) has greater 
2- vs. 1-
selectivity than clonidine and causes more 2-selective vasoconstriction in the human
forearm. Following local 
-adrenergic blockade with propranolol, forearm blood flow (FBF; plethysmography) responses to brachial artery administration of Dex, clonidine, and phenylephrine (1-agonist) were determined in healthy young adults before and after 2-blockade with yohimbine (n = 10) or 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) and this effect was abolished by yohimbine and blunted by
prazosin. These results suggest that Dex causes more 2-selective vasoconstriction in the forearm than clonidine. The similar vasoconstrictor responses to both drugs after prazosin might be explained by the pre-synaptic effects on norepinephrine release.
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