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PubMed1961

Effect of noradrenaline, bretylium and cocaine on the blood pressure response to tyramine in the rat.

Tyramine is mainly a pressor agent in the rat under urethane, although the hypertensive effect of tyramine in some experiments is followed by a prolonged increase or depression of blood pressure. Bretylium, in doses up to 10 mg/kg, prolonged the response to tyramine, whereas larger doses depressed or blocked its effect. When the hypertensive effect of tyramine was blocked by bretylium, both noradrenaline and dihydroxyphenylalanine, when slowly infused, were found to restore it. The well-known block by cocaine of the hypertensive response to tyramine could also be reversed by intravenous infusion of noradrenaline and dihydroxyphenylalanine. It is concluded that the infusion of noradrenaline and dihydroxyphenylalanine makes available noradrenaline in the postganglionic adrenergic nerves which is necessary for the action of tyramine.

Animals↗
PubMed1990

Hypotensive action and weak potentiation of tyramine effect by moclobemide in rats.

Moclobemide belongs to a new class of reversible, selective monoamine oxidase-A (MAO-A) inhibitors; it is clinically well tolerated and has little liability to potentiate tyramine pressor effects. Measurement of blood pressure and heart rate in conscious, freely moving rats showed only a slight, nonsignificant decrease in mean arterial pressure in normotensive animals. However, in spontaneously hypertensive rats, moclobemide significantly decreased blood pressure by 20 mmHg within 30 min of oral intake of 30 mg/kg. In the same animals, heart rate was decreased by 20%; normal values returned after 2-3 h. Tyramine alone in oral doses up to 15 mg/kg had no effect on blood pressure in normotensive rats, and after treatment with 30 mg/kg moclobemide, tyramine at 5 mg/kg did not alter mean arterial pressure, whereas there was a significant increase after doses of tranylcypromine, toloxatone and brofaromine. Higher doses of tyramine (10-20 mg/kg) following moclobemide led to a rise of 30-40 mmHg in pressure, but this had disappeared within 20 min. This effect was almost completely eliminated by desipramine, suggesting that coadministration of a norepinephrine uptake inhibitor with a reversible MAO inhibitor is likely to reduce the risk of tyramine-induced hypertensive crisis. Thus, the authors conclude that moclobemide exerts only a slight hypotensive action in hypertensive rats, and differs from other MAO inhibitors in potentiating the pressor effect of tyramine only weakly.

Administration, Oral↗
PubMed1977

Intravenous tyramine response in migraine before and during treatment with indoramin.

We studied the response of 31 migraine sufferers (20 women, 11 men) to intravenous tyramine (the tyraminedose)pressor response test). Patients were treated either with pacebo tablets or indoramin, and alpha-adrenergic blocking agent, in a double-blind crrossover trial. We found that patients with migraine required significantly less tyramine to increase their cystolic blod pressure by 30 mm Hg when compared with matched controls. Indoramin significantly increased the amount of tyramine needed to raise the systolic blood pressure among migraine suffers and reduced the incidence of posttyramine migraine for m 46% while patients were on placebo tablets to 8% when they were receiveing indoramin. There was no association between tyramine sensitivity and a history of premenstrual or dietary migraine, nor was there a significant difference in the indierenence in the incidence of post-tyramine migrain between men women. We conclude that the intravenous tyramine test may be valuable in assessing migraine suffers who will respond to an alpha-advenergic blocking agent such as indoramin.

Blood Pressure↗
PubMed1972

Effect of tyramine in migraine: a double-blind study.

The incidence of headache and changes in the EEG after tyramine were studied in 25 migrainous patients in a double-blind placebo-controlled investigation. There were three groups of patients: the first had migraine alone, the second had migraine and epilepsy, and the third had migraine which was precipitated by food substances containing tyramine. Psychological tests showed that all the patients were more neurotic, more introverted, and more obsessional than normal subjects. Headache occurred in 12 of 50 patient sessions and 10 of these occurred in the group with dietary precipitated migraine. In this group, however, headache followed tyramine alone in only two patients. The remaining eight headaches occurred in two patients after placebo alone, and in three after both test capsules. The EEG was activated after tyramine, but not after placebo, in 11 of the 15 patients with migraine and epilepsy, and dietary precipitated migraine. This effect was observed, however, in only two of the 10 patients with classical migraine alone. There was no relation between the occurrence of headache and EEG activation. Although there was no significant relationship between tyramine ingestion and the occurrence of headache, the EEG changes observed during the study support the hypothesis that tyramine has an action on the central nervous system in some migrainous subjects.

Adult↗
PubMed1986

Concentration of striatal tyramine and dopamine metabolism in diabetic rats and effect of insulin administration.

Earlier work has shown that diabetic rats possess lower concentrations of brain p-tyrosine; these animals also show a decrease in the rate of accumulation of striatal DOPA after decarboxylase inhibition and an increase in striatal binding sites for dopamine. These findings suggested that diabetic rats show a reduction in the metabolism of brain dopamine. This is an investigation of the effects of streptozotocin-induced (65 mg/kg, intracardially) diabetes on rat striatal concentrations of p-tyrosine, p-tyramine, m-tyramine, dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid. Also, the effects of insulin administration (0.5-4 IU/kg, intraperitoneally) to normal and diabetic rats were studied. The onset of diabetes or effect of insulin treatment was determined by the changes produced in blood glucose. Streptozotocin produced a significant reduction in the striatal concentration of p-tyrosine, 3,4-dihydroxyphenylacetic acid and homovanillic acid observed 7 or 14 days after injection. The treatment produced a reduction in p-tyramine and an increase in m-tyramine. Insulin administration significantly increased rat striatal p-tyrosine, p-tyramine, 3,4-dihydroxyphenylacetic acid and homovanillic acid while m-tyramine was decreased. The concentrations of p-tyrosine, dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid in the striatum of insulin-treated diabetic rats were within the range of control values. The results indicate that streptozotocin-diabetic rats possess a reduced striatal dopamine metabolism and that this is counteracted by insulin administration. These changes are probably the consequence of changes in the availability of some amino acid precursors and in tyrosine hydroxylase activity.

3,4-Dihydroxyphenylacetic Acid↗
PubMed2005

Differences in alpha 1-adrenoceptor subtype-mediated vasoconstriction by tyramine and nerve stimulation in canine splenic artery.

This study was designed to clarify the alpha(1)-adrenoceptor subtypes mediating the vasoconstrictor response to tyramine in isolated and perfused canine splenic artery. It was shown that tyramine potentiated the nerve stimulation-induced second peaked vasoconstriction that was readily suppressed by prazosin treatment. A bolus injection of tyramine (0.01-0.3 micromol) caused a vasoconstriction in a dose-related manner. The tyramine-induced vasoconstriction was inhibited by WB 4101 (10 and 100 nM), an alpha(1A)-and alpha(1D)-adrenoceptor antagonist, in a concentration-related manner. Neither BMY 7378 (100 nM), a selective alpha(1D)-adrenoceptor antagonist, nor chloroethylclonidine (60 microM), an alpha(1B)- and alpha(1D)-adrenoceptor antagonist, affected the tyramine-induced response. The results indicate that the noradrenaline released by tyramine may diffuse to the extrajunctional cleft, and thus it activates the extrajunctional alpha(1A)-adrenoceptors, because nerve stimulation-evoked second peaked vasoconstrictions were markedly inhibited by chloroethylclonidine but not by WB 4101.

Adrenergic Fibers↗
PubMed1988

Differential responsiveness of LH and prolactin to p-tyramine in male and female rats.

The effect of p-tyramine, a natural amine which is found in the rat brain in trace amounts, was evaluated for its capacity to influence LH and prolactin secretion in male and female rats under different hormonal conditions. p-Tyramine (40 mg/kg ip) was ineffective in modifying LH levels in either female or male rats which had been gonadectomized for 2 days, but if the animals were injected with 12.5 micrograms of estradiol benzoate (EB) on the day of castration, p-tyramine was able to release LH in female but not in male rats. To evaluate whether early androgenization of brain structures which control LH secretion was involved in the sexual difference observed, p-tyramine was tested in female androgenized rats (200 micrograms of testosterone propionate on the day of birth), and in male rats castrated at birth. The trace amine was ineffective in altering LH levels in both experimental models, even if rats were pretreated with EB as control females. On the other hand, p-tyramine inhibited prolactin secretion in male rats pretreated with EB, and not in similarly treated female rats. The present results suggest that p-tyramine may be involved not only in prolactin regulation as it has been previously shown, but also in LH control, and that the hormonal response to this amine is sexually differentiated in the rat.

Animals↗
PubMed1976

Treatment of neurogenic orthostatic hypotension with a monoamine oxidase inhibitor and tyramine.

The clinical response of treatment with a chemical preparation of tyramine and tranylcypromine, a monoamine oxidase inhibitor, is described in six patients wit neurogenic orthostatic hypotension. Previous therapy with fluorocortisone, ephedrine, elastic garments, postural training and, in one patient, an anti-G suit was unsuccessful. Oral and intravenous tyramine produced no pressor response. However, after treatment with tranylcypromine five of the patients when supine showed a marked rise of blood pressure to intravenous tyramine which was sustained for over two hours when they stood up. Tyramine given orally with tranylcypromine produced a moderate rise of blood pressure in the supine position which was sustained for over 3-4 hours in the erect position enabling patients to walk about without symptoms of orthostatic hypotension. Measurement of circulating adrenaline and noradrenaline during therapy suggested that the pressor response was due to release of noradrenaline. Three patients have had marked improvement for four, fifteen and twenty-four months respectively. In a further patient, therapy has been successful in treating his orthostatic hypotension although his mobility has been restricted due to cerebellar ataxia. One patient developed a confusional state during treatment and the therapy was stopped. The only patient in whom the drugs produced no pressor response had orthostatic hypotension with evidence of adrenergic innervation of blood vessels, but failure of noradrenaline release. It is suggested that the pressor response to a monoamine oxidase inhibitor and tyramine should be examined in patients to a monoamine oxidase inhibitor and tyramine should be examined in patients with neurogenic orthostatic hypotension in whom conventional therapy is unsatisfactory and those who respond should receive a trial of this treatment.

Blood Pressure↗
PubMed1976

Biosynthesis and metabolism of endogenous tyramine and its normal presence in sympathetic nerves.

By use of a sensitive and specific enzymatic isotopic method for the determination of tyramine, the small quantities of this amine which are present endogenously in rat tissues, including brain, heart, kidney and salivary gland, have been quantitated. The levels of tyramine in brain were increased to a similar extent by injecting animals with a monoamine oxidase inhibitor, pargyline, and a dopamine beta-hydroxylase inhibitor, FLA-63; in contrast, pretreatment of animals with alpha-methyl-para-tyrosine, a tyrosine hydroxylase inhibitor, did not lead to an increase in tyramine levels in brain. Pretreatment of rats with 6-hydroxydopamine resulted in a marked diminution in the tyramine content of rat atria and salivary gland. Denervation of the salivary gland decreased the endogenous level of tyramine approximately 50% in denervated glands compared to undenervated glands. These results suggest that tyramine exists at least partly in sympathetic nerves in many tissues.

Animals↗
PubMed1990

The effect of various monoamine oxidase (MAO) inhibitors on the response of blood pressure of rats and cats to tyramine.

The "cheese effect" is the clinically most important side effect of structurally different MAO inhibitors. It occurs mainly as a result of the interaction of MAO inhibitor with tyramine in foodstuffs. Anaesthetised rats and cats were used in order to investigate and compare the influence of the effect of tyramine by selective MAO type-B inhibitors with that produced by non-selective and A-selective MAO inhibitors on the one hand, and on the other hand, different MAO-B inhibitors with (-)deprenyl. (-)Deprenyl was the only one which inhibited the effect of tyramine in the experimental animals used, while other MAO inhibitors potentiated the tyramine effect. Therefore this study indicates that not only non-selective and A-selective inhibitors potentiate the effect of tyramine but selective inhibitors of B-type MAO as well. The inhibition of tyramine uptake by (-)deprenyl is a remarkable exception from the rule.

Anesthesia↗
PubMed1978

The effects of some stimulants and anti-psychotic drugs on urinary unconjugated tyramine levels in the rat.

The effects of intraperitoneal injections of amphetamine and methylphenidate (ritalin) at relatively low and high doses, the anti-psychotic drugs chlorpromazine and haloperidol and combinations of haloperidol with methylphenidate and amphetamine on the urinary excretion levels of unconjugated meta and para tyramine in the rat have been investigated. With the exception of a high dose of methylphenidate, none of the drug treatments changed significantly the urinary excretion level of para tyramine. meta Tyramine was significantly reduced by a low dose of amphetamine and a high dose of methylphenidate but significantly increased by a high dose of amphetamine. Such effects are different from those reported by Juorio (1977a, b) and Danielson, et al (1976) with respect to the rat striatum and mesolimbic systems where para tyramine was decreased and meta tyramine increased. The effect of adding anti-psychotic drugs in these latter studies was to potentiate their differential effects. Such differences indicate perhaps variations in the metabolism of the tyramines in peripheral tissues as compared with certain brain regions.

Animals↗
PubMed1995

The effect of enalapril on tyramine induced changes in renal function in man.

Increasing animal evidence support an important facilitatory interaction between angiotensin II and norepinephrine within the kidney. This angiotensin II/norepinephrine interaction was investigated in man by examining the effect of enalapril pretreatment (5 mg for 5 days) on the renal response to a low non-pressor dose of intravenous tyramine 4 micrograms/kg/min for 120 min in 8 healthy subjects undergoing water diuresis. Tyramine is an indirect sympathomimetic agent which causes neuronal release of norepinephrine. Enalapril and tyramine, alone and in combination, had no effect on glomerular filtration, effective renal plasma flow or sodium excretion. Tyramine caused a significant increase in urinary flow rate (p < 0.05) but this was not influenced by enalapril pretreatment. The lack of effect of enalapril on the renal response to tyramine contrasts with a previous study which examined the effect of enalapril on the renal response to circulating norepinephrine. This may suggest that enalapril affect renal function only when there is renal vasoconstriction (as with norepinephrine) and not when renal blood flow is unchanged (as with tyramine).

Adult↗
PubMed1995

[Level of histamine and tyramine in ripening cheeses].

Histamine poisoning is a foodborne chemical intoxication resulting from the ingestion of food products containing high levels of histamine. Historically, histamine poisoning has been attributed to the consumption of fish species belonging to the Scomberesocidae and Scombridae families and other sea fish, but histamine poisoning outbreaks may occur after the consumption of cheese, or other types of fermented foods. Also tyramine has been proved as a cause of adverse reactions, involving headache, hypertensive crisis and interactions with antidepressive drugs, which were observed after consumption of ripening cheeses. The formation of high levels of histamine and tyramine in foods is directly correlated to the level of microorganisms, possessing the enzymes: histidine and tyrozyne decarboxylases, and also with the concentration of histidine and tyrosine free substrate. Proteolysis, which takes place during ripening of cheeses may play role in the release of free histidine and tyrosine. This study reports on the levels of histamine and tyramine in ripening cheeses taken from Polish food market. 43 samples of soft and hard cheeses were investigated. Histamine was measured according to the AOAC fluorometric method. Tyramine was measured after column separation and purification, according to the spectrofluorometric technique with 1-nitroso-2-ortophtalate aldehyde, according to Carou with couple of modifications by authors. Histamine levels ranged from 0 to 157 mg/kg and tyramine levels ranged from 3.8 to 575 mg/kg. The very high levels of histamine and tyramine in many samples of cheeses support the opinion, that sometimes the storage temperature has not been sufficient to stop bacterial multiplication and in consequence enzymatic activity of decarboxylases of native amino acids--precursors of biogenic amines in ripening cheeses.

Cheese↗
PubMed1998

Tyramine and vanadate synergistically stimulate glucose transport in rat adipocytes by amine oxidase-dependent generation of hydrogen peroxide.

Nonadrenergic imidazoline I2-binding sites colocalize with monoamine oxidase (MAO) in various tissues. As white adipocytes from various species have been reported to be very rich in I2-sites, the authors consider whether these cells show a substantial MAO activity and explore its functional role. Oxidation of [14C]tyramine by rat adipocyte membranes was dependent on both MAO and semicarbazide-sensitive amine oxidase (SSAO). Tyramine oxidation was identical in membranes and in intact adipocytes (Vmax: 11-12 nmol/min/mg protein). A similar effect of MAO and SSAO inhibitors was obtained in both the intact cells and the membranes: half of the activity was sensitive to semicarbazide and the other half more easily inhibited by MAO-A than by MAO-B inhibitors. As the reaction catalyzed by amine oxidases generates H2O2, which mimicks certain insulin effects in adipocytes, we tested whether tyramine oxidation influences glucose transport in adipocytes. One mM tyramine weakly stimulated glucose transport. A clear potentiation of tyramine effect occurred in the presence of 0.1 mM vanadate, ineffective by itself, reaching half-maximal insulin stimulation. This stimulation was sensitive to MAO and SSAO inhibitors and to catalase. The 5-fold activation of glucose transport was accompanied by translocation of GLUT4 transporters to the plasma membrane. This shows that tyramine is readily oxidized by adipocytes and potentiates the effects of vanadium on glucose transport through release of hydrogen peroxide. The role of the amine oxidases, which are highly expressed in adipocytes, allows them to be considered as more than mere scavengers of circulating amines.

Adipocytes↗
PubMed1982

Pinocytosis of poly (alpha, beta-(N-2-hydroxyethyl))-DL-aspartamide and a tyramine derivative by rat visceral yolk sacs cultured in vitro. Ability of phenolic residues to enhance the rate of pinocytic capture of a macromolecule.

Incorporation of 20% tyramine residues into its structure greatly increased the rate of pinocytosis of poly(alpha, beta-(N-2-hydroxyethyl))-DL-aspartamide (PHEA) by rat visceral yolk sacs cultured in vitro. Both the parent macromolecule and the tyramine derivative (PHEA-tyramine) were captured by adsorptive pinocytosis, the higher affinity of the derivative for the yolk sac plasma membrane being responsible for its greater rate of capture. Using 125I-labelled PHEA-tyramine, the relationship between substrate concentration and rate of capture was determined, it was also shown that following internalization, the PHEA-tyramine linkage is resistant to intracellular hydrolysis. Fluorescence micrographs were consistent with capture of both substrates being by pinocytosis and illustrated the highly efficient concentration of the tyramine derivative by yolk sac endodermal cells.

Animals↗
PubMed1964

RELATIVE ACTIONS OF QUATERNARY METHYL DERIVATIVES OF TYRAMINE, DOPAMINE AND NORADRENALINE.

Tyramine methiodide and dopamine methobromide have greater pressor effect (three- to five-times) in the spinal cat than the parent amines. Noradrenaline methochloride has little pressor effect. Dopamine methobromide is about four times as potent as nicotine; tyramine methiodide is about equiactive to nicotine; and noradrenaline methochloride has only one-tenth the potency of nicotine. Their pressor effects are usually abolished by hexamethonium but in some experiments the effect of noradrenaline methochloride persisted and was then abolished by tolazoline. Injected intravenously into the cat anaesthetized with chloralose, each of the three quaternary derivatives contracts the nictitating membrane; dopamine methobromide is again the most active, having more than six times the potency of nicotine. When the contractions of the nictitating membrane are induced by continuous stimulation of the preganglionic fibres of the cervical sympathetic nerve, intravenous injection of the quaternary derivatives of tyramine and dopamine has a biphasic effect; there is a block on which a contraction of the membrane appears to be superimposed. Noradrenaline methochloride produces only a further contraction of the membrane. On the isolated rectus abdominis muscle preparation of the frog, dopamine methobromide is the most active in contracting the muscle, being about twelve times as active as nicotine; noradrenaline methochloride is weakest, having only one-hundredth the activity of nicotine. These effects are antagonized by hexamethonium. On the isolated phrenic nerve-diaphragm preparation of the rat, the quaternary derivatives of tyramine and dopamine each have neuromuscular blocking properties, 0.7- and 3-times respectively that of nicotine. Noradrenaline methochloride has no effect. In the sciatic nerve-tibialis preparation of the cat, the quaternary derivatives of tyramine and dopamine are approximately equipotent in producing neuromuscular paralysis, having about three times the activity of nicotine and one-fifth that of suxamethonium. These effects are not antagonized either by neostigmine or by edrophonium. Noradrenaline methochloride has no neuromuscular blocking effect. The nicotine-like properties of these quaternized sympathomimetic amines are discussed. It is of interest that the presence of an hydroxyl group attached to the beta-carbon atom of the side-chain greatly reduces nicotine-like activity. By comparison, choline had about one forty-fifth the pressor activity of ethyltrimethylammonium.

Ammonium Compounds↗
PubMed1987

The metabolism of ingested deuterium-labelled p-tyramine in normal subjects.

Eight normal subjects ingested 125 mg of p-tyramine-beta,beta-2H2 hydrochloride and the 3 h and following 21 h urine collections were analysed by mass spectrometry with selected ion monitoring for the deuterated metabolites: free and conjugated p-tyramine-beta,beta-2H2, free p-octopamine-beta-2H1, free and conjugated p-hydroxyphenylacetic acid-alpha-2H1 and -alpha,alpha-2H2, and free p-hydroxymandelic acid-alpha-2H1. These metabolites accounted for 72% of the ingested label, of which conjugated p-tyramine and free p-hydroxyphenylacetic acid constituted 90%. Approximately 50% of the total deuterated tyramine and 70% of the total deuterated p-hydroxyphenylacetic acid were excreted in the first three hours, although there was considerable variation between individuals. The presence of a small amount of p-hydroxyphenylacetic acid-alpha-2H1 suggests that some exchange of deuterium occurred at the intermediate p-hydroxyphenylacetaldehyde stage. These results, based as they are on metabolites labelled with the stable isotope deuterium, ought to be more reliable than earlier studies in which unlabelled tyramine was ingested with the resultant metabolites, indistinguishable from their endogenous metabolic counterparts, being measured by fluorimetry or gas chromatography.

Administration, Oral↗
PubMed1991

Effect of a novel monoamine-oxidase inhibitor, moclobemide on the sensitivity to intravenous tyramine and norepinephrine in humans.

This study compared the effects of moclobemide (Ro11-1163), a selective and reversible inhibitor of monoamine-oxidase (MAOI) type A and phenelzine, an irreversible non-selective MAOI, on the pressor responses to IV tyramine and norepinephrine. Because of the reversibility of this inhibition, the pressor effect of tyramine was expected to be minimal. Twelve healthy men participated in this randomized double-blind, placebo-controlled, crossover study. Volunteers began with oral treatment of moclobemide (100 mg TID) or phenelzine (15 mg TID) for 1 week followed by placebo treatment for 2 weeks and then moclobemide or phenelzine treatment for another week. The tyramine and norepinephrine challenge tests were conducted at baseline and then at weekly intervals, for a total of five challenges. The average tyramine dose that was required to increase systolic blood pressure by 25 mm Hg (PD25) was 1.6 +/- 0.2 mg after moclobemide treatment, which was lower (P less than .01) than the baseline value of 3.6 +/- 0.7 mg and that after phenelzine (3.0 +/- 0.5 mg) treatment. Moclobemide did not influence norepinephrine sensitivity. In conclusion, moclobemide mildly decreased the sensitivity to IV tyramine as compared with placebo and phenelzine.

Adult↗