Seven normotensive patients with
alcohol amnestic disorder were treated with 2 micrograms/kg
clonidine (C) three times daily for 1 wk. Four patients received 12 micrograms/kg/day during the subsequent week; three developed hypotensive symptoms at this dose and remained on 6 micrograms/kg/day. During a predrug placebo period and after 60 hr on each dose of C, urinary excretion rates of
catecholamine metabolites were determined. C, 6 micrograms/kg/day, reduced the ratio of
norepinephrine (NE) metabolites (mumol/24 hr) to
normetanephrine (NM),
vanillylmandelic acid (VMA), and 3-methoxy-4-hydroxyphenyl glycol (
MHPG). The excretion of
metanephrine (M) was not reduced significantly. The ratio M/NM and M/(VMA +
MHPG) increased, indicating Cs effects are primarily noradrenergic. Reduction in NM/(VMA +
MHPG) indicates disproportionate lowering of the O-methylated metabolite of NE compared to its deaminated metabolites, consistent with C inhibition of NE release. Patients with the highest predrug NM excretion had the greatest decrements with C. The
dopamine metabolites
3-methoxytyramine and
homovanillic acid were not decreased by C. C-induced reductions in the ratio NM/(VMA +
MHPG), an index of NE release, correlated (n = 7) with reductions in supine systolic blood pressure, mean arterial pressure, and salivary flow rate.