Submitted on March 7, 2005
Accepted on July 18, 2005
Clonidine induces nitric oxide and prostaglandin mediated vasodilation in healthy human skin
Daniel Hermann1, Tanja Schlereth1, Thomas Vogt1, and Frank Birklein1*
1 Department of Neurology, University of Mainz, Mainz, Germany
* To whom correspondence should be addressed. E-mail: birklein{at}neurologie.klinik.uni-mainz.de.
Sustained sympathetic activation leads not only to vasoconstriction but might also induce paradox vasodilation. This study was performed to explore whether and how 
2-receptor (2-R) stimulation mediates this vasodilation. We investigated eleven 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, 5x10-4, 10-4 mol/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 NMMA and ASA induced vasoconstriction (p<0.001). By co-application of CL 10-3 mol/L with NMMA or ASA vasodilation was
partially prevented (p<0.001). Our results demonstrate that sustained 2-R stimulation induces vasodilation in a dose dependent way, which is mediated by nitric oxide and prostaglandin mechanisms in human skin.
