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Comparison of the effects of chronic administration of ciclazindol and desipramine on pupillary responses to tyramine, methoxamine and pilocarpine in healthy volunteers.
Author(s) -
Kerr FA,
Szabadi E
Publication year - 1985
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1985.tb02691.x
Subject(s) - methoxamine , desipramine , miosis , mydriasis , pilocarpine , anesthesia , medicine , pharmacology , endocrinology , agonist , antidepressant , epilepsy , receptor , psychiatry , hippocampus
Twenty‐nine healthy volunteers participated in an experiment lasting for 8 weeks: Phase I (2 weeks)‐pre‐treatment control period; Phase II (4 weeks)‐medication with either ciclazindol hydrochloride (50 mg twice daily), or desipramine hydrochloride (50 mg twice daily) or lactose placebo (twice daily) administered in a single‐blind fashion; Phase II (2 weeks)‐recovery. Experimental sessions took place twice weekly for the photographic assessment of resting pupil diameter, and for the assessment of one of the following pupillary responses: mydriatic response to methoxamine, mydriatic response to tyramine, miotic response to pilocarpine. Resting pupil diameter increased during medication with either ciclazindol or desipramine. Methoxamine‐evoked mydriasis and tyramine‐evoked mydriasis were antagonized by both ciclazindol and desipramine. Pilocarpine‐evoked miosis was potentiated by both ciclazindol and desipramine. The steady‐state plasma levels (mean +/‐ s.e. mean) of the antidepressants were: ciclazindol: 5.90 +/‐ 0.74 microM; desipramine: 0.60 +/‐ 0.17 microM. The antagonism of methoxamine‐evoked mydriasis is likely to reflect the blockade of postsynaptic alpha 1‐adrenoceptors in the iris by the antidepressants, whereas the antagonism of tyramine‐evoked mydriasis may reflect both the blockade of uptake of tyramine into presynaptic adrenergic terminals and the blockade of postsynaptic alpha‐adrenoceptors. There is no immediate explanation for the potentiation of pilocarpine‐evoked miosis by the two antidepressants.