Abstract
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 language | English (US) |
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Pages (from-to) | 587-592 |
Number of pages | 6 |
Journal | Journal of applied physiology |
Volume | 99 |
Issue number | 2 |
DOIs | |
State | Published - Aug 2005 |
Keywords
- Forearm blood flow
- Resistance vessels
- Sympathetic nervous system
- Vasoconstriction
ASJC Scopus subject areas
- Physiology
- Physiology (medical)