Dissociation of norepinephrine turnover from alpha-2 responses after clorgiline.
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 alpha 2-receptor function as measured by responses to clonidine are modest and highly variable. Furthermore, since the variable and inconsistent changes in alpha 2-receptor function are dissociated from the massive changes in norepinephrine metabolism, regulation of presynaptic alpha 2-receptors appears unlikely to mediate the effects of clorgiline in patients with depression.[1]References
- Dissociation of norepinephrine turnover from alpha-2 responses after clorgiline. Hauger, R.L., Scheinin, M., Siever, L.J., Linnoila, M., Potter, W.Z. Clin. Pharmacol. Ther. (1988) [Pubmed]
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