Effects of clonidine on central and peripheral catecholamine metabolism

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Abstract
CSF (n = 5) and plasma (n = 7) levels of norepinephrine (NE) and its major metabolite, 3-methoxy-4-hydroxyphenylglycol (MHPG), were examined in abstinent normotensive men with alcohol amnestic disorder during placebo and after 2 wk of clonidine [a hypotensive, sympatholytic agent] treatment (6 or 12 .mu.g/kg per day). Clonidine reduced concentrations of NE and both free and total MHPG in CSF and plasma. The CNS contribution to CSF free MHPG also decreased (as estimated from the differential reductions in CSF and plasma levels). Percent reductions in CSF and plasma NE were substantially greater than those for MHPG, suggesting diminished CNS and peripheral NE release and turnover. CSF levels of homovanillic acid (HVA), which is derived solely from CNS dopamine metabolism, rose in each patient, whereas the CSF serotonin metabolite, 5-hydroxyindoleacetic acid, did not change. The increase in HVA cannot be attributed to inhibition of acid transport from brain to blood. Changes in central noradrenergic and dopaminergic activity correlated inversely; diminished NE release and enhanced dopamine metabolism may be contribute to the effects of clonidine in man.