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]References
- 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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