Although originally developed for the treatment of hypertension, alpha(2)-agonists have been used to treat Tourette's syndrome, attention-deficit hyperactivity disorder (ADHD), developmental disorders and substance abuse for nearly three decades. Based on studies of clonidine, alpha(2)-agonists were presumed to reduce arousal by decreasing the firing of noradrenaline neurons in locus ceruleus. Accumulated preclinical evidence indicates that guanfacine has features in common with clonidine, in addition to other pharmacological effects. Clonidine binds to the three subtypes Of alpha(2)-receptors, A, B and C, whereas guanfacine binds more selectively to alpha(2A)-receptors, which appears to enhance prefrontal function. Several reports on the use of the alpha(2)-agonists show improvements in children with ADHD and improvements in hyperactivity, impulsiveness and inattention in children with tic disorders and pervasive developmental disorders. Both clonidine and guanfacine are associated with sedation, fatigue and somnolence. Reductions in heart rate and blood pressure are modest and rarely lead to discontinuation of treatment across these trials.
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