Urinary catecholamine metabolites and effects of clonidine in patients with alcohol amnestic disorder

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Abstract
Clonidine (C) is the prototype of a class of antihypertensive drugs thought to act primarily through central .alpha.2-adrenergic receptors to decrease sympathetic outflow from the CNS. Seven normotensive patients with alcohol amnestic disorder were treated with 2 .mu.g/kg C, 3 times daily for 1 wk. Four patients received 12 .mu.g/kg per day during the subsequent week; 3 developed hypotensive symptoms at this dose and remained on 6 .mu.g/kg per day. During a predrug placebo period and after 60 h on each dose of C, urinary excretion rates of catecholamine metabolites were determined. C at 6 .mu.g/kg per day reduced the ratio of norepinephrine (NE) metabolites (.mu.mol/24 h) 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 that C 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.

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