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Effects of clonidine on central and peripheral catecholamine metabolism
Author(s) -
Martin Peter R,
Ebert Michael H,
Gordon Edna K,
Linnoila Markku,
Kopin Irwin J
Publication year - 1984
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1984.37
Subject(s) - homovanillic acid , endocrinology , clonidine , medicine , metabolite , dopamine , norepinephrine , catecholamine , cerebrospinal fluid , dopaminergic , chemistry , metabolism , serotonin , receptor
Cerebrospinal fluid (CSF; n = 5) and plasma (n = 7) levels of norepinephrine (NE) and its major metabolite, 3‐methoxy‐4‐hydroxyphenyl glycol (MHPG) were examined in abstinent normotensive men with alcohol amnestic disorder during placebo and after 2 wk of Clonidine treatment (6 or 12 µg/kg/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. Thus 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; thus diminished NE release and enhanced dopamine metabolism may both contribute to the effects of Clonidine in man. Clinical Pharmacology and Therapeutics (1984) 35, 322–327; doi: 10.1038/clpt.1984.37