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Dissociation of norepinephrine turnover from alpha‐2 responses after clorgiline
Author(s) -
Hauger Richard L,
Scheinin Mika,
Siever Larry J,
Linnoila Markku,
Potter William Z
Publication year - 1988
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.1988.8
Subject(s) - norepinephrine , endocrinology , medicine , clonidine , chemistry , adrenergic receptor , heart rate , alpha (finance) , receptor , blood pressure , dopamine , construct validity , nursing , patient satisfaction
Responses to intravenous clonidine, a possible central noradrenergic probe, were examined in patients with depression before and after treatment with clorgiline, a selective monoamine oxidase type A inhibitor. Pulse rate, mean arterial blood pressure, plasma norepinephrine, 3‐methoxy‐4‐hydroxyphenylglycol, and growth hormone were measured. Clorgiline treatment (2.5 to 10 mg/day) produced a variable reduction in the hypotensive response to clonidine but did not influence heart rate or plasma norepinephrine responses. Clorgiline markedly reduced the urinary output of norepinephrine and metabolites, indicating a reduced turnover of norepinephrine. None of the measured parameters corresponded with clinical effect. These data suggest that any clorgiline‐induced alterations in α 2 ‐receptor function as measured by responses to clonidine are modest and highly variable. Furthermore, since the variable and inconsistent changes in α 2 ‐receptor function are dissociated from the massive changes in norepinephrine metabolism, regulation of presynaptic α 2 ‐receptors appears unlikely to mediate the effects of clorgiline in patients with depression. Clinical Pharmacology and Therapeutics (1988) 43, 32–38; doi: 10.1038/clpt.1988.8