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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

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

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.[1]


  1. Urinary catecholamine metabolites and effects of clonidine in patients with alcohol amnestic disorder. Martin, P.R., Ebert, M.H., Gordon, E.K., Kopin, I.J. Clin. Pharmacol. Ther. (1983) [Pubmed]
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