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PubMed1985

Comparison of the effects of chronic administration of ciclazindol and desipramine on pupillary responses to tyramine, methoxamine and pilocarpine in healthy volunteers.

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.

Adolescent↗
PubMed1982

The effect of some precursor amino acids and enzyme inhibitors on the mouse striatal concentration of tyramines and homovanillic acid.

The parenteral administration of L-phenylalanine or p-tyrosine increases the mouse striatal concentration of p-tyramine, an effect that is enhanced by monoamine oxidase inhibition and reduced by an L-aromatic aminoacid decarboxylase inhibitor. Striatal m-tyramine was increased following administration of L-phenylalanine or m-tyrosine and enhanced further by monoamine oxidase inhibition. It was also observed that m-tyrosine is a better substrate for decarboxylation than p-tyrosine, and that p-tyrosine decarboxylation was blocked by NSD 1055, while that of m-tyrosine was enhanced. The results obtained indicate that both isomers of tyramine are formed in the mouse striatum by hydroxylation of L-phenylalanine to p- or m-tyrosine followed by decarboxylation by a specific decarboxylase; an alternative pathway could be first the decarboxylation of phenylalanine to beta-phenylethylamine, followed by its hydroxylation to p- or m-tyramine.

Animals↗
PubMed1989

Interaction between moclobemide and oral tyramine in depressed patients.

We investigated the pressor response to oral tyramine before and during treatment with moclobemide, a selective monoamine oxidase-A inhibitor, in 10 depressed patients. Before moclobemide therapy, tyramine was associated with a mean (SD) maximum rise in systolic blood pressure of 4.0 (5.2) mmHg, whereas during moclobemide treatment, tyramine was associated with an increase of 24.9 (14.2) mmHg. Only one subject failed to demonstrate an increased pressor response while taking moclobemide. Moclomebide potentiates the pressor response to oral tyramine, but is safer than older nonselective monoamine oxidase inhibitors.

Adult↗
PubMed1961

Effect of noradrenaline on the action of nicotine and tyramine on isolated atria.

Both nicotine (in the presence of atropine) and tyramine cause a rise in the rate of isolated rabbit atria. When noradrenaline is allowed to act on the atria for 20 to 30 min and then removed from the bath by repeated changes of the bath fluid, the action of nicotine and of tyramine is greatly increased. The first addition of noradrenaline to the bath often has a much smaller effect on the response to nicotine or to tyramine than have later additions. Sometimes the greater effect after the addition of nicotine persists for 2 or 3 hr. When reserpine is added to the bath and left in contact with the atria for 1 to 2 hr, and is then removed from the bath, the effect of noradrenaline on the atrial rate is much reduced in size and duration. Bretylium abolishes the action of nicotine but increases the action of tyramine.

Animals↗
PubMed1962

On the mechanism of tachyphylaxis to tyramine in the isolated rat heart.

Tyramine was shown to release [(3)H]-catecholamines from an isolated rat heart previously perfused with [(3)H]-noradrenaline. With successive injections of tyramine the amount of [(3)H]-catecholamine released fell progressively and there was a parallel decrease in the increment of amplitude and rate of contraction of the heart. Reserpinized hearts were shown to take up less [(3)H]-noradrenaline than normal hearts. Release of radioactivity and loss of responsiveness to tyramine occurred more rapidly in the reserpinized heart. In the same preparation the uptake of [(14)C]-tyramine exceeded the quantity of the noradrenaline released.

Animals↗
PubMed1968

Restoration of the chronotropic effect of tyramine on rat atria after reserpine.

1. The restoration by various sympathomimetic amines of the chronotropic response to tyramine was studied on the isolated atria of rats pretreated with reserpine. The atria were exposed to the "restorative" sympathomimetic amine for 10 min, washed over a period of 1 hr and then tested with 10 muM tyramine. The effect of noradrenaline, dopamine and norphenylephrine before and after inhibition of monoamine oxidase by 0.5 mM iproniazid were compared with their alpha-methyl and N-alkyl analogues in their ability to restore the chronotropic response to tyramine.2. Noradrenaline and adrenaline restored the chronotropic response to tyramine, the degree of restoration depending on the concentration of the restorative amine used. Noradrenaline after iproniazid and alpha-methylnoradrenaline were equipotent and were about 1,000 times more active than noradrenaline where monoamine oxidase was not inhibited. Dopamine, epinine, norphenylephrine, phenylephrine, octopamine, synephrine and isoprenaline in the absence of monoamine oxidase inhibition had no effect. Dopamine after iproniazid and alpha-methyldopamine were equipotent and were about 1/10 as active as alpha-methylnoradrenaline. Norphenylephrine after iproniazid and metaraminol were equipotent and were about 1/500 as active as alpha-methylnoradrenaline. Octopamine after iproniazid was even less active. The N-methylated analogues were about 1/10 as active as their nor-compounds but the N-isopropyl analogue, isoprenaline, was devoid of activity.3. Dopamine after iproniazid and alpha-methyldopamine were inactive if a dopamine-beta-hydroxylase inhibitor, disulphiram or sodium diethyldithiocarbamate, was present.4. It is concluded that, in atria of reserpinized rats, (a) protection from monoamine oxidase increases; (b) N-substitution decreases; and (c) hydroxyl groups at the beta-carbon and ring positions 3 and 4 increase the capabilities of a sympathomimetic amine to restore the chronotropic response to tyramine.

Animals↗
PubMed1968

Interaction between desipramine, tyramine, and amphetamine at adrenergic neurones.

1. Small doses of tyramine (10 mug/kg intravenously) are taken up by rat heart, which can concentrate the amine 7.3-fold over the plasma level.2. Desipramine (DMI) blocks the uptake of small doses of tyramine by rat heart, but in doses of 20 mg/kg intraperitoneally, it does not affect the cardiac concentrations of tyramine following 20 mg/kg intramuscularly of the drug. The same dose of DMI prevents the depletion of noradrenaline (NA) elicited by intramuscular injection of tyramine 20 mg/kg.3. DMI prevents the depletion of heart NA elicited by (+)-amphetamine 5 mg/kg given intraperitoneally to demedullated rats and enhances the heart concentration of amphetamine.4. Liposoluble amphetamine enters sympathetic nerves by simple diffusion. It is suggested that DMI prevents the release of heart NA caused by this indirect sympathomimetic through an action within the adrenergic neurone.

Amphetamine↗
PubMed1982

The effect of gamma-hydroxybutyrate on mouse striatal tyramine, dopamine and homovanillic acid.

1 The concentrations of p- and m-tyramine, dopamine and homovanillic acid were measured in the mouse striatum following the subcutaneous injection of gamma-hydroxybutyrate; their control levels were 19.8, 6.3, 9600 and 1130 ng/g respectively. 2 The administration of 500-1000 mg/kg of gamma-hydroxybutyrate produced a reduction in p-tyramine that lasted at least 8 h. m-Tyramine and dopamine were significantly increased for at least 4 h. The levels of homovanillic acid were increased at 1 and 2 h after drug administration. 3 There experiments strongly suggest that the increases in dopamine turnover produced by gamma-hydroxybutyrate caused reciprocal changes in striatal tyramine that are similar to those produced by drug or treatment that increase dopamine turnover and tyrosine hydroxylase activity.

Animals↗
PubMed1990

Relationship between tyramine potentiation and monoamine oxidase (MAO) inhibition: comparison between moclobemide and other MAO inhibitors.

The pharmacodynamic properties of moclobemide, a reversible inhibitor of MAO-A (RIMA), were compared with the properties of other reversible as well as older irreversible MAO inhibitors in human subjects. All the substances supposed to have MAO-A-inhibitory activity, with the exception of toloxatone, were shown by the decrease in plasma DHPG or MHPG levels to cause inhibition ranging between 50% and 85%. Toloxatone and low doses of deprenyl (a MAO-B inhibitor) caused 20% and 17% inhibition respectively; higher doses of deprenyl, however, strongly inhibited MAO-A. MAO-B inhibition was confirmed for all nonselective and selective MAO-B inhibitors. Moclobemide and clorgyline were found to be the most highly selective MAO-A inhibitors, although both also inhibited 30% of platelet MAO-B activity. Potentiation of the tyramine pressor effect is mainly influenced by the irreversibility and degree of MAO-A inhibition. Tyramine sensitivity was raised (a factor of 10-30) by all irreversible MAO inhibitors in doses inhibiting MAO-A; it diminished with increasing reversibility. In therapeutic doses, moclobemide potentiated the intravenous tyramine pressor effect 3 times less than the old irreversible MAO inhibitors; with the highest therapeutic dose, the tyramine sensitivity factor for moclobemide is only one-seventh to one-tenth that of tranylcypromine or phenelzine. Duration of action is obviously also closely related to the reversibility of inhibition: it ranged from up to 2 days with high doses of moclobemide to 3 weeks with tranylcypromine; clorgyline and phenelzine have been shown to maintain their action for several months. The new generation of RIMAs represents a significant progress in safety.(ABSTRACT TRUNCATED AT 250 WORDS)

Antidepressive Agents↗
PubMed1980

Thermoregulatory responses to tyramine in the pigeon.

Intravenous injections of different doses of tyramine induced hypothermia in the pigeon in the cold and a moderate hyperthermia in the warm environment. The hypothermia was correlated with a dose-dependent decline in shivering. Hyperthermia was attributed to the chrono- and inotropic effects of tyramine. The indirect stimulatory effects of noradrenaline (NA) at the tissue level were studied. Pretreatment with alpha-methyl-para-tyrosine (alpha-MpT) and blocking alpha-adrenoceptors with phentolamine, diminished the hypothermia induced by tyramine in the cold. The results obtained indicate that the release of endogenous NA stimulated by tyramine might result either in hypothermia or hyperthermia, thus resembling similar effects obtained with exogenous NA in birds.

Animals↗
PubMed1980

Genetic control of tyramine oxidase, which is involved in derepressed synthesis of arylsulfatase in Klebsiella aerogenes.

Mutants of Klebsiella aerogenes with three types of mutations affecting regulation of tyramine oxidase were isolated by a simple selection method. In the first type, the mutation (tynP) was closely linked to the structural gene for tyramine oxidase tynA). The order of mutation sites was atsA-tynP-tynA. In the second type, the mutation that relieves catabolite repression of the syntheses of several catabolite repression-sensitive enzymes are not linked to the tyn gene by P1 transduction. These strains contained high levels of cyclic adenosine 5'-monophosphate when grown on glucose. The third type of mutation, in which tyramine oxidase was synthesized constitutively, was shown by genetic analysis to involve mutations of tynP and tynR. The tynR gene was not linked to tynA. Results using the constitutive mutants showed that the constitutive expression of the tynA gene resulted in depression of arylsulfatase synthesis in the absence of tyramine.

Arylsulfatases↗
PubMed1982

Precursors and metabolites of phenylethylamine, m and p-tyramine and tryptamine in human lumbar and cisternal cerebrospinal fluid.

Phenylacetic acid, p-hydroxyphenylacetic acid, m-hydroxyphenylacetic acid, phenylalanine, indoleacetic acid, 5-hydroxyindoleacetic acid and tryptophan were measured in lumbar and cisternal cerebrospinal fluid (CSF) taken during pneumoencephalography. The data suggest that the concentration of the acid metabolites of the trace amines tryptamine, phenylethylamine, p-tyramine and m-tyramine in lumbar CSF are influenced by the system that transports these acids out of CSF. In cisternal CSF this mechanism does not operate and more information can be obtained on the metabolism of the parent amines in the CNS. Our data indicate that (1) m-tyramine is relatively unimportant quantitatively (2) the rate of metabolism of phenylethylamine in human brain is similar to that of 5-hydroxytryptamine (3) the most important variable controlling the synthesis of phenylethylamine is the activity of aromatic amino acid decarboxylase (4) p-tyramine is synthesised at about half the rate of phenylethylamine and is thus quantitatively important in metabolic terms.

Adolescent↗
PubMed1983

Pressor sensitivity to tyramine in patients with headache: relationship to platelet monoamine oxidase and to dietary provocation.

The pressor responses to oral and intravenous tyramine were not different from controls in migrainous patients with or without a history of attacks triggered by foods. However, patients who reported a dietary trigger were more likely to develop headache after tyramine administration than those without such a dietary history. Pressor responses to intravenous tyramine in patients with cluster headache were indistinguishable from controls. A group of five males with platelet monoamine oxidase activity one standard deviation or more below that of male controls required less intravenous tyramine to raise blood pressure by 30 mm Hg than males with monoamine oxidase levels within one standard deviation of the controls. This finding suggests that platelet monoamine oxidase activity to some extent reflects that of total body monoamine oxidase A plus B.

Administration, Oral↗
PubMed1981

Endogenous norepinephrine release induced by tyramine modulates intestinal ion transport.

To study the effects of endogenous norepinephrine on intestinal ion transport, we tested the actions of an indirect sympathomimetic agent, tyramine, on electrolyte fluxes in the short-circuited rabbit ileum in vitro. Tyramine (10(-5) M) alone had no effect on short-circuit current or Na transport but increased Cl absorption. Tyramine decreased the short-circuit current, stimulated both Na and Cl absorption, and increased tissue conductance when its breakdown by endogenous monoamine oxidase enzymes was inhibited by pretreatment with pargyline (10(-4) M). Pargyline alone had no effect on short-circuit current and NaCl transport. The effect of norepinephrine on NaCl transport was inhibited by the alpha-adrenergic receptor antagonist, phentolamine (10(-7) M). This response was also prevented when animals were chemically sympathectomized with 6-hydroxydopamine. Although sympathectomy decreased measurable tissue norepinephrine by 80%, it did not alter basal short-circuit current, Na and Cl absorption, and the short-circuit current response to glucose-stimulated Na transport and to exogenous norepinephrine. Thus, a pool of norepinephrine in intestinal adrenergic neurons released by tyramine affects intestinal ion transport but does not alter basal ion transport. These data suggest close neuropharmacologic similarities between the adrenergic nervous system in the intestine and other organs.

Animals↗
PubMed1993

The effects of tyramine on salivary flow rate and protein secretion by rat submandibular glands.

The effects of different doses of p-tyramine injected i.v. and i.p. on salivary flow rates and proteins secreted by the submandibular glands of rats were studied with and without various types of autonomic blockers and two enzyme inhibitors. The salivary flow rates and the amounts of protein secreted progressively increased with increasing doses injected both i.v. and i.p., whereas they were dramatically reduced with all autonomic blockers except the lowest doses of beta-blockers, atropine, and yohimbine. Salivation in response to p-tyramine injected i.v. and i.p. was completely abolished by simultaneous injections of both prazosin and propranolol. The concentration of protein was not dose-dependent and was not reduced by yohimbine and phenoxybenzamine at almost all doses used. However, prazosin significantly increased the protein concentration. Protease activities were dose-dependent but were significantly reduced with alpha-blockers other than yohimbine, and with most beta-blockers. The proteins secreted in response to p-tyramine at all doses injected i.v. and i.p. were of the alpha-type except with the lowest dose injected i.p. However, the alpha-type was completely replaced by the beta-type in the presence of all alpha-blockers except yohimbine, but not with beta-blockers, atropine, or two enzyme inhibitors. Pargyline, a monoamine-oxidase inhibitor, but not disulfiram, a dopamine-beta-hydroxylase inhibitor, affected all parameters except the type of protein. Thus, p-tyramine may activate both the alpha 1- and beta 1-adrenoceptors in the submandibular glands of rats directly or indirectly.

Adrenergic alpha-Antagonists↗
PubMed2003

An improved protocol of biotinylated tyramine-based immunohistochemistry minimizing nonspecific background staining.

An immunohistochemical method using biotinyl tyramine was recently introduced to amplify weak staining signals. Despite its high sensitivity, however, tyramine-based immunostaining has been limited by its increased background staining. In this study, to develop an improved protocol of biotinyl tyramine-based immunohistochemistry minimizing the background staining, we determined which staining steps lead to the nonspecific reaction and the most appropriate blocking agents for background-provoking steps. Trypton casein peptone and distilled water with Tween-20 were shown to be most effective as a blocking agent and a rinsing solution, respectively. In conclusion, we developed an optimized protocol for biotinyl tyramine-based immunohistochemistry with minimal background staining.

Biotin↗
PubMed1998

Degradation of histamine and tyramine by Brevibacterium linens during surface ripening of Munster cheese.

Red smear formation during fermentation of Munster cheese was started by using three different strains of Brevibacterium linens as surface inocula. The cheeses were produced with and without supplementation of histamine and tyramine. After smearing the cheese surface for the first time with B. linens viable counts of 10(7) CFU/g were detected. At the end of the logarithmic growth phase cell numbers increased to 10(10) CFU/g and remained constant during the whole ripening period. During a 4-week ripening period strains of B. linens reduced histamine and tyramine content by 55 to 70%. B. linens LTH 456 and LTH 3686 degraded histamine and tyramine in a phosphate buffer (pH 7) containing 0.54 M histamine and 0.58 M tyramine when incubated with agitation at 30 degrees C. B. linens LTH 3813 did not reveal any amine degradation activity in a buffer system. The pH on the cheese surface increased from 5 to 7, whereas it increased in the center only to 5.3 after a 3-week ripening period.

Biodegradation, Environmental↗
PubMed1992

[Age effects of topical tyramine and cocaine on the pupil].

In order to obtain the age distribution of normal values of the effects of topical tyramine or cocaine on the pupil, we measured the pupillary light reflexes of 50 normal volunteers before and 45 minutes (tyramine) or 90 minutes (cocaine) after the topical instillation in right eyes. Left eyes were used as controls. An infrared videopupillogram (HTV-C301) was used. Topical tyramine as well as cocaine caused mydriasis, increase of maximum %-velocity of dilatation (%-VDmax), reduction of %-amplitude of constriction (%-A) and decrease of maximum %-velocity of constriction (%-VCmax). These alternations of pupillary parameters coincided with the changes induced by topical epinephrine. The effects of tyramine or cocaine significantly increased as the age of the subjects increased, though the increase of %-VDmax caused by cocaine was only related to age. Age-related augmentation of pupillary changes were also been observed in a previous study using topical epinephrine or topical pilocarpine which concluded that the effects of any topical autonomics were increased by aging. No physiological senile Horner's syndrome was detected. It was concluded that the age-related augmentation of pupillary changes caused by topical autonomics probably resulted from the increment of corneal permeability in the aged which was confirmed in the previous fluorophotometric study by the authors following topical fluorescein administration. It is possible to assess the pupillary sensitivity to topical adrenergics of the patients with bilateral Horner's syndrome by comparing the age-related normal values obtained in this study.

Adolescent↗