The interaction of tyramine with a single dose of tranylcypromine in healthy volunteers.

Peet, Malcolm; Yates, R A; Carroll, JA; Middlemiss, D.N.

doi:10.1111/j.1365-2125.1981.tb01127.x

Cited by 6 publications

(2 citation statements)

References 12 publications

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“…Furthermore, it has been reported that the mydriatric response to tyramine is enhanced in patients receiving chronic treatment with the MAO inhibitors iproniazid, isocarboxazid and clorgyline [20],and benmoxine [21]. However, two previous studies, using single doses of classical irreversible nonselective MAO inhibitors (phenelzine [22], tranylcypromine [23]), failed to demonstrate the potentiation of tyramine‐evoked mydriasis in healthy volunteers, although in both studies there was evidence for the potentiation of the tyramine‐evoked pressor response.…”

Section: Introductionmentioning

confidence: 99%

Comparison of the effects of moclobemide and selegiline on tyramine‐evoked mydriasis in man

Bitsios

Langley

Tavernor

et al. 1998

Brit J Clinical Pharma

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Aims To examine the feasibility of using the human iris in vivo for the assessment of the interaction between tyramine and monoamine oxidase (MAO) inhibitors. To examine the relative roles of the two forms of MAO in terminating the response to sympathomimetic amines in the iris, by comparing the effects of single oral doses of moclobemide, a selective MAO-A inhibitor, and selegiline, a selective MAO-B inhibitor, on mydriatic responses to tyramine. Methods Twelve healthy male volunteers participated in three monthly sessions, each associated with ingestion of one capsule (moclobemide 450 mg, selegiline 10 mg, or placebo), according to a double-blind, balanced, cross-over design. Tyramine hydrochloride eye-drops (75 mm, 2×10 ml) were instilled three times in the left conjuctival sac at 40 min intervals. Pupil diameter was monitored with a binocular infrared television pupillometer before and for 4.5 h after ingestion of the capsule. The pupillary response to tyramine was expressed as the area under the pupil diameter×time curve (arbitrary units). A blood sample was taken before and 2 h after ingestion of the capsule, for the assay of platelet MAO-B activity, and plasma 3,4-dihydroxyphenylglycol (DHPG) concentration, an index of MAO-A activity. Platelet MAO activity was assayed radiochemically, using [14 C]-phenylethylamine as substrate, and plasma DHPG by high performance liquid chromatography (h.p.l.c.). The results were analysed using analysis of variance with repeated measures, followed by Bonferroni's corrected t-test, using a significance criterion of P<0.05. Results Both moclobemide and selegiline, compared with placebo, caused significant miosis in the right (untreated) eye. The changes in pupil diameter (mm±s.e. mean) from the pretreatment measurement were: placebo −0.09±0.07, moclobemide −0.52±0.09, selegiline −0.26±0.1. The mydriatic response to tyramine was potentiated by moclobemide, compared with the response recorded in the presence of placebo. The responses to tyramine (arbitrary units±s.e. mean) were: placebo 77.08±11.65, moclobemide 140.25±18.9, selegiline 72.75±12.35. Both moclobemide and selegiline significantly reduced platelet MAO activity, compared with placebo. The changes in platelet MAO activity (nmol h −1 mg −1 protein±s.e. mean) from the pretreatment level were: placebo 0.5±0.62, moclobemide −6.7±0.66, selegiline −17.7±0.87. Moclobemide significantly reduced plasma DHPG concentration, compared with placebo. The changes in plasma DHPG concentration (nmol l −1 ±s.e. mean) from the pretreatment level were: placebo −0.01±0.24, moclobemide −4.98±0.32, selegiline −0.51±0.26. Conclusions The potentiation of tyramine-evoked mydriasis by moclobemide is likely to reflect the inhibition of MAO-A activity in the iris, consistent with the activity of this enzyme in sympathetic nerve terminals. The lack of effect of selegiline on tyramine-evoked mydriasis argues against a role of MAO-B in terminating the effects of sympathomimetic amines in the iris. The effects of the two drugs on platelet MAO activi...

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Section: Introductionmentioning

confidence: 99%

Comparison of the effects of moclobemide and selegiline on tyramine‐evoked mydriasis in man

Bitsios

Langley

Tavernor

et al. 1998

Brit J Clinical Pharma

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“…It is likely that PLZ inhibits its own metabolism (Danielson et al 1984), as is evidenced by the gradual accruement of steady-state plasma levels over the first 6 to 8 weeks of chronic administration (Baker et al 1999;Robinson et al 1985); this may clarify why Trembath and Turner (1979) observed no TYR potentiation following administration of a single dose of PLZ-a finding Peet et al (1981) attributed to 'the relative lack of potency in man (…) in comparison to (TCP)'. The present theory posits instead that PLZ does engender notable such effects, albeit following an initial delay (Baker et al 1984).…”

Section: Plz: Select Topics Of Metabolismmentioning

confidence: 99%

The trace amine theory of spontaneous hypertension as induced by classic monoamine oxidase inhibitors

Eynde¹

2021

J Neural Transm

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The classic monoamine oxidase inhibitors (MAOIs) tranylcypromine (TCP) and phenelzine (PLZ) are powerful antidepressants that come with an equally powerful stigma, and are thus rarely prescribed-despite their well-established effectiveness. Some of these preconceptions appear to stem from unclarity, as the etiology of a rare but important side effect, 'spontaneous hypertension' (SH)-a significant increase in blood pressure absent dietary tyramine ingestion-remains improperly elucidated. This paper aims at uprooting some of the stigma surrounding MAOIs by advancing the trace amine (TA) theory as the causative underpinning of SH. This theory posits that SH results from the considerable influx of TAs observed following TCP-or PLZ-administration. TAs are known, albeit at greatly supraphysiological levels, to raise blood pressure on account of their propensity to exert potent indirect sympathomimetic effects; additionally, some research posits that TAs may induce vasoconstrictive effects partly or wholly separate therefrom, which would then constitute a second hypertensive mechanism. TAs are endogenous to the human body in low quantities. Both TCP and PLZ cause marked elevations of 2-phenylethylamine (PEA), meta-and para-tyramine (m-/p-TYR), octopamine (OA), and tryptamine (TRYP), following both acute and (sub) chronic administration. This paper holds that TYR plays a pivotal role in causing SH, due to its strong pressor effect. Cautious treatment of SH is advised, given its typically self-limiting nature. The risk of hypotensive overshoots must be taken into account. For severe cases, this paper urges reconsideration, following suitable confirmation trials, of antipsychotics (notably risperidone) as these agents may reduce striatal p-TYR levels.

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The use of monoamine oxidase inhibition to estimate megakaryocyte-platelet regeneration time (MPRT)

Chamberlain

Tong

Chiu

et al. 1988

Thrombosis Research

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The interaction of tyramine with a single dose of tranylcypromine in healthy volunteers.

Cited by 6 publications

References 12 publications

Comparison of the effects of moclobemide and selegiline on tyramine‐evoked mydriasis in man

Comparison of the effects of moclobemide and selegiline on tyramine‐evoked mydriasis in man

The trace amine theory of spontaneous hypertension as induced by classic monoamine oxidase inhibitors

The use of monoamine oxidase inhibition to estimate megakaryocyte-platelet regeneration time (MPRT)

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