Selective α2-adrenergic properties of dexmedetomidine over clonidine in the human forearm

Shizue Masuki, Frank A. Dinenno, Michael J. Joyner, John H. Eisenach

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47 Scopus citations


We tested the hypothesis that dexmedetomidine (Dex) has greater α2- vs. α1 selectivity than clonidine and causes more α2-selective vasoconstriction in the human forearm. After local β-adrenergic blockade with propranolol, forearm blood flow (plethysmography) responses to brachial artery administration of Dex, clonidine, and phenylephrine (α1-agonist) were determined in healthy young adults before and after α2-blockade with yohimbine (n = 10) or α1-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 α2-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.

Original languageEnglish (US)
Pages (from-to)587-592
Number of pages6
JournalJournal of applied physiology
Issue number2
StatePublished - Aug 2005


  • Forearm blood flow
  • Resistance vessels
  • Sympathetic nervous system
  • Vasoconstriction

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)


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