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J Appl Physiol 99: 2266-2270, 2005. First published July 21, 2005; doi:10.1152/japplphysiol.00271.2005
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Clonidine induces nitric oxide- and prostaglandin-mediated vasodilation in healthy human skin

Daniel Hermann, Tanja Schlereth, Thomas Vogt, and Frank Birklein

Department of Neurology, University of Mainz, Mainz, Germany

Submitted 7 March 2005 ; accepted in final form 18 July 2005

Sustained sympathetic activation not only leads to vasoconstriction but also might induce paradox vasodilation. This study was performed to explore whether and how {alpha}2-receptor stimulation mediates this vasodilation. We investigated 11 healthy subjects in 33 dermal microdialysis (MD) sessions. After nerve trunk blockade, MD fibers were inserted and perfused with physiological saline until skin trauma-related vasodilation subsided. Thereafter, fibers were perfused with either clonidine solutions (10–3, 5 x 10–4, 10–4 mol/l), NG-monomethyl-l-arginine (L-NMMA; nitric oxide synthase blocker), acetylsalicylic acid (ASA; cyclooxygenase blocker), or combinations of these. Laser-Doppler scanning of the investigated skin revealed that clonidine not only induces vasoconstriction but subsequently also vasodilation with higher concentrations (P < 0.001). In contrast, both L-NMMA and ASA induced vasoconstriction (P < 0.001). By coapplication of 10–3 mol/l clonidine with L-NMMA or ASA, vasodilation was partially prevented (P < 0.001). Our results demonstrate that sustained {alpha}2-receptor stimulation induces vasodilation in a dose-dependent way, which is mediated by nitric oxide and prostaglandin mechanisms in human skin.

dermal microdialysis; sympathetic nervous system; alpha-adrenoreceptors; laser-Doppler imaging


Address for reprint requests and other correspondence: F. Birklein, Neurologische Klinik, Universität Mainz, Langenbeckstrasse 1, D-55101 Mainz, Germany (e-mail: birklein{at}neurologie.klinik.uni-mainz.de)






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