The Mechanism of the Augmentation of Responses to Indirectly Acting Sympathomimetic Amines by Monoamine Oxidase Inhibitors

Rand, M. J.; Trinker, Fedora R.

doi:10.1111/j.1476-5381.1968.tb00990.x

Cited by 28 publications

(13 citation statements)

References 45 publications

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“…Experimental evidence suggests that another mechanism by which MAO inhibitors enhance the pressor effect of tyramine is by retarding its metabolism in the liver (28). However, intravenckis tyramine was not augmented by tranylcypromine in either patient; this is contrasted with the marked hypertensive response produced by oral cheese (tyramine) during monoamine oxidase inhibition.…”

Section: Discussioncontrasting

confidence: 47%

Idiopathic postural hypotension: physiologic observations and report of a new mode of therapy

Diamond¹,

Murray²,

Schmid³

1970

J. Clin. Invest.

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A B S T R A C T Two patients with severe postural hypotension associated with upper motor neuron and cerebellar impairment (Shy-Drager syndrome) have been studied. Head-up tilt and lower body negative pressure application caused marked falls in arterial pressure; in one patient, paradoxical vasodilatation was observed. Ice application did not increase arterial pressure or calculated forearm vascular resistance. Intravenous atropine in one patient increased heart rate by 18 beats per min, a cardioacceleratory response similar to exhausting recumbent exercise in that patient. 24 hr urinary catecholamine excretion was low, but aldosterone secretory rate was normal in the more severely afflicted patient. A prolonged elevation of plasma renin activity was noted when post-tilt hypertension occurred. When head-up tilt was not followed by this hypertensive period, plasma renin activity response to tilting was normal. Intraarterial norepinephrine and tyramine both elicited a vasoconstrictor response. Intra-arterial infusions of norepinephrine and tyramine were repeated after administration of the monoamine oxidase inhibitor tranylcypromine. Norepinephrine was potentiated 4.1-and 0.5-fold in the two patients; tyramine was potentiated 3.7-and 1.1-fold in the two patients, respectively. A therapeutic program of tranylcypromine and tyramine (in the form of cheddar cheese) resulted in substantial clinical improvement. It is concluded that in at least some patients with idiopathic postural hypotension, norepinephrine is present in postganglionic sympathetic fibers. A therapeutic program of tyramine and a monoamine oxiThis work was presented in part at

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Section: Discussioncontrasting

confidence: 47%

Idiopathic postural hypotension: physiologic observations and report of a new mode of therapy

Diamond¹,

Murray²,

Schmid³

1970

J. Clin. Invest.

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“…It was stated that the drugs to be used with caution include adrenaline and noradrenaline. Although there was some evidence of potentiation of the pressor effects of these catecholamines by monoamine oxidase inhibitors (Harrer et al, 1964;Fischbach et al, 1966), other workers found no evidence of potentiation either in animals (Rand and Trinker, 1968) or in man (Horwitz et al, 1960;Elis et al, 1967).…”

Section: Introductionmentioning

confidence: 99%

Interactions between Sympathomimetic Amines and Antidepressant Agents in Man

Boakes¹,

Laurence²,

Teoh³

et al. 1973

BMJ

133

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SummaryIntravenous infusions of phenylephrine, noradrenaiine, adrenaline, and isoprenaline were given to healthy human volunteers after five to seven days on phenelzine, tranylcypromine, or imipramine, and cardiovascular responses were compared with those observed under control conditions. With monoamine oxidase inhibitors there was a 2-2k fold potentiation of the pressor effect of phenylephrine, but no clinically significant potentiation of cardiovascular effects of noradrenaline, adrenaline, or isoprenaline. With imipramine there was potentiation of the pressor effects ofphenylephrine (2-3 fold), noradrenaline (4-8 fold), and adrenaline (2-4 fold); there were dysrhythmias during adrenaline infusions, but no noticeable or consistent changes in response to isoprenaline.Noradrenaline and adrenaline in amounts contained in local anaesthetics used in dentistry are not likely to be significantly potentiated in otherwise healthy patients receiving monoamine oxidase inhibitors. Hazardous potentiation of their cardiovascular effects might occur in patients receiving tricyclic antidepressants.Our observations do not indicate that the hazards associated with isoprenaline inhalation by bronchial

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“…2). Tranylcypromine does not potentiate the effects of catecholamines on the cardiovascular system; in fact, it reduces them slightly (Trinker, Fearn & others, 1967;Rand & Trinker, 1968). The appearance of the secondary pressor effect of histamine after tranylcypromine, as shown in Fig.…”

Section: Figmentioning

confidence: 89%

“…These doses produced marked potentiation of cardiovascular responses to tyramine and amphetamine (Rand & Trinker, 1968).…”

Section: E X P E R I M E N T a Lmentioning

confidence: 98%

Interaction between histamine and monoamine oxidase inhibitors

Allen

Rand

1969

Journal of Pharmacy and Pharmacology

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The Mechanism of the Augmentation of Responses to Indirectly Acting Sympathomimetic Amines by Monoamine Oxidase Inhibitors

Cited by 28 publications

References 45 publications

Idiopathic postural hypotension: physiologic observations and report of a new mode of therapy

Idiopathic postural hypotension: physiologic observations and report of a new mode of therapy

Interactions between Sympathomimetic Amines and Antidepressant Agents in Man

Interaction between histamine and monoamine oxidase inhibitors

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