anything that leads to increased norepinephrine will lead to increased VMA in the urine. (similarly, increased dopamine --> increased HVA in urine, increaed epinephrine --> increased metanephrines in urine). all of these metabolites can be interconverted via COMT, etc. see: http://homepages.gac.edu/~cellab/chpts/chpt7/Images/fig7_6.gif
of the ones you listed, i would pick imipramine. in addition to being norepi reuptake inhibitors, TCAs have anti-adrenergic effects and you might see a compensatory increase in catecholamines to maintain homeostasis.
-fluphenazine is a SRI, leads to increase Serotonin and then possibly 5-HIAA
-benztropine is an anticholineric and antihistaminic treatment for Parkinsonism, competes with Ach which physiologically antagonizes the indirect/negative feedback pathway in the basal ganglia, and is also used to ameliorate antipsychotics (which increase nor/epinephrine levels)... I don't think it actually raises the levels of endogenous ligands
-amantadine is a weak Glutamate/NMDA-R antagonist used to treat parkinsonism, and thus will increase dopamine release/level, to be metabolized into HVA, but you'd expect some rise in VMA also
-fluoxetine is an SSRI (Prozac) which can be expected to increase levels of Serotonin and thus 5-HIAA
-imipramine is a tricyclic which inhibits reuptake of a bunch of ****, most notably NE. NE metabolizes to VMA, so I guess this is the best answer.
Since Fluphenazine and Fluoxetine are similar, cross those out.. Benztropine is an antagonist not a reuptake inhibit, and then so is Amantadine, although apparently that induces a feedback loop to increase Dopamine. Imipramine everyone remembers as tricyclic for mostly NE, so that would be the best answer.