The mechanism of action of<unk>  is not fully clear. Although it is a centrally acting sympathomimetic, it does not block reuptake or transporters. It may reduce the dopaminergic and serotonergic transmission in the peripheral nervous system and it indirectly affects norepinephrine (noradrenaline) synthesis.<unk>  acts on alpha-2 adrenergic receptors, which are found on the pre synaptic nerve terminal. This inhibits the synthesis of norepinephrine by inhibiting tyrosine hydroxylase. The S-enantiomer of<unk>  is a competitive inhibitor of the enzyme aromatic L-amino acid decarboxylase (LAAD), which converts L-DOPA into dopamine. L-DOPA can cross the blood brain barrier and thus<unk>  may have similar effects. LAAD converts it into alpha-methyldopamine, a false prescursor to norepinephrine, which in turn reduces synthesis of norepinephrine in the vesicles. Dopamine beta hydroxylase (DBH) converts alpha-methyldopamine into alpha-methylnorepinephrine, which is an agonist of the presynaptic α2-adrenergic receptor causing inhibition of neurotransmitter release.
Methyldopa
Fluorodopa
Cortisone
Galantamine
Acotiamide
Alpha-Hydroxyetizolam
Metergoline
Levothyroxine