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PubMed1994

Release of endogenous ATP from the vasa deferentia of the rat and guinea-pig by the indirect sympathomimetic tyramine.

1. Adenosine 5'triphosphate (ATP) as well as [3H]-noradrenaline ([3H]-NA) is released by perfusion of the vas deferens with the indirect sympathomimetic tyramine (100 microM); this result is consistent with the concept of sympathetic cotransmission. 2. While tyramine produced a strong contraction in the vas deferens of the rat, it had little mechanical action in the guinea-pig vas deferens. This appears to be largely because tyramine induces considerably lower levels of release of both ATP and NA from the guinea-pig vas deferens compared to that of the rat. Furthermore, NA released by tyramine appears to release ATP from a secondary pool in the rat vans deferens, but not that of the guinea-pig, since prazosin reduced the tyramine-induced release of ATP in the rat vas deferens. 3. alpha,beta-Methylene ATP (alpha,beta-meATP) increased both the spontaneous release of ATP and the tyramine-evoked efflux of ATP and [3H]-NA. The basal and tyramine-induced efflux of [3H]-NA was also enhanced by the alpha 1-adrenoceptor antagonist, prazosin, suggesting that prejunctional alpha 1-adrenoceptors may modulate neurotransmitter release.

Adenosine Triphosphate↗

PubMed1962

An investigation of the action of tyramine and its interrelationship with the effects of other sympathomimetic amines.

Choline 2,6-xylyl ether potentiated the sympathomimetic effects of tyramine and adrenaline in anaesthetized and spinal cats; the effects of noradrenaline were not significantly affected. The pressor activity of tyramine was also potentiated by the drug in reserpine-treated spinal cats and in pithed rats. The acute intravenous injection of reserpine in pithed rats potentiated pressor responses to tyramine, but depressed those to adrenaline and noradrenaline. During the intravenous infusion of noradrenaline in spinal cats and pithed rats the pressor responses to tyramine were increased, whilst those to adrenaline and noradrenaline were decreased. Infusion of isoprenaline in a spinal cat depressed responses to tyramine and noradrenaline, but potentiated those to adrenaline. A lower rate of infusion of isoprenaline in the same animal subsequently potentiated adrenaline and noradrenaline, but continued to depress tyramine. These results are held to be inconsistent with the view that the sympathomimetic effects of tyramine are produced entirely by the release of catechol amines.

Amines↗

PubMed1962

Effect of tyramine on isolated guinea-pig atria in relation to their noradrenaline stores.

The relation between the noradrenaline content of isolated guinea-pig atria and the rate-increasing action of tyramine was studied by the use of pretreatment with reserpine as a pharmacological tool for graded depletion of the noradrenaline stores. Reserpine was more potent in depleting the stores than in reducing the biological response to tyramine; 50% depletion had little effect on the response to tyramine; 50% reduction of the response to tyramine occurred when the noradrenaline content fell to about 10% of normal. Depletion of the stores of guinea-pig atria did not result in supersensitivity to noradrenaline. Exposure of heavily pretreated atria to 3 x 10(-6) noradrenaline for 10 min (followed by repeated washing for 45 min) restored the response to tyramine to 70% of normal; it failed, however, to restore the noradrenaline content to the level expected from the experiments with reserpine alone. Restoration of the response to tyramine was accompanied by a small but significant increase in the noradrenaline content of the atria; a change in sensitivity to added noradrenaline did not occur. The results are consistent with the view that (a) the noradrenaline stores consist of two compartments the smaller of which is important for the action of tyramine, that (b) this smaller compartment can be at least partially refilled by exposure of the atria to noradrenaline, and that (c) there is no direct relationship between the noradrenaline content and the sensitivity to noradrenaline in guinea-pig atria.

Guinea Pigs↗

PubMed1981

Tyramine antagonistic properties of AGN 1135, an irreversible inhibitor of monoamine oxidase type B.

1 The effects of the irreversible monoamine oxidase (MAO) inhibitors, AGN 1133, AGN 1135 and (-)-deprenyl, on tyramine and noradrenaline responses and uptake of [3H]-metaraminol were investigated in the isolated vas deferens of the rat. Uptake of [3H]-metaraminol and [3H]-octopamine was compared in mouse vas deferens. The modification of tyramine and noradrenaline-induced pressor responses by AGN 1133 and AGN 1135 was examined in anaesthetized rats and cats. 2 AGN 1133 (7.5 x 10(-6)M) greatly potentiated responses to tyramine in the rat isolated vas deferens. Both AGN 1135 and (-)-deprenyl inhibited tyramine responses selectively at concentrations above 10(-5)M (which caused almost complete inhibition of MAO types A and B) but tyramine responses were potentiated on washing out the inhibitors. 3 AGN 1135 (10(-4)M) and (-)-deprenyl (10-5)M) inhibited [3H]-metaraminol uptake by about 20% in rat and mouse vas deferens; neither inhibitor affected [3H]-octopamine uptake in mouse vas deferens. Desmethylimipramine (10(-6)M) inhibited amine uptake by more than 70%. 4 AGN 1133 (1.5 mg/kg) potentiated pressor responses to tyramine in rats and cats whereas AGN 1135 (1.5 mg/kg) did not. 5 AGN 1135 possesses tyramine antagonistic activity which is qualitatively similar to that of (-)-deprenyl but which cannot satisfactorily be explained by inhibition of neuronal or granula amine uptake.

Animals↗

PubMed1990

Interaction between orally administered tyramine and moclobemide.

This article describes a standardized oral tyramine pressor test designed to give information on safety aspects in the real everyday life situation where tyramine is ingested only with food. Results showed that significantly higher doses of tyramine were required to raise standing blood pressure by at least 30 mmHg (TYR 30) when it was taken with food than when subjects fasted. The same test was then conducted in 8 healthy volunteers during treatment with moclobemide 200 mg 3 times daily and tranylcypromine 10 mg 3 times daily. With moclobemide the mean TYR 30 dose was 306 mg, and the ratio of this to baseline was 5.0. With tranylcypromine, however, the mean TYR 30 dose was only 35 mg and the TSF ratio 38.2. The potentiation by tranylcypromine was thus 7.6 times greater than that of moclobemide. When tyramine was given in the food under treatment with MAO inhibitors, the TYR 30 doses were larger than those obtained under fasting conditions, but the TSF ratios were not altered. When the tyramine was given in a protein-rich or a lipid-rich meal, the previously established TYR 30 had significantly less effect on the blood pressure. The lowest TYR 30 dose during moclobemide treatment is at least 150 mg tyramine, an amount contained in about 300 g strong cheese or 100 g of yeast extract. These quantities are unlikely to be consumed in a normal meal. The corresponding TYR 30 dose for tranylcypromine, however, is only 20 mg tyramine, which can easily be contained in a fairly normal portion of strong cheese (40 g).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1973

Derepression of arylsulfatase synthesis in Aerobacter aerogenes by tyramine.

Studies were made on the effect of tyramine on arylsulfatase synthesis in mutants of Aerobacter aerogenes ATCC 9621 deficient in enzymes involved in tyramine degradation. As shown previously, some sulfur compounds, such as inorganic sulfate, repressed enzyme synthesis while others, such as methionine, did not. Tyramine caused derepression of enzyme synthesis, which is repressed by inorganic sulfate. The present work showed that, although tyramine readily derepressed arylsulfatase synthesis, metabolites of tyramine in either the wild-type or mutant strains did not, so that the derepression is due to the particular structure of tyramine. Kinetic studies on the cells indicated that incorporation of sulfur into protein and enzyme synthesis occurred on supply of either a sulfur compound, which did not cause repression, or of tyramine, which caused derepression, irrespective of the type of sulfur compound added, if any.

Carbon Radioisotopes↗

PubMed2002

Regulation of chloride permeability by endogenously produced tyramine in the Drosophila Malpighian tubule.

The Malpighian (renal) tubule of Drosophila melanogaster is a useful model for studying epithelial transport. The purpose of this study was to identify factors responsible for modulating transepithelial chloride conductance in isolated tubules. I have found that tyrosine and several of its metabolites cause an increase in chloride conductance. The most potent of these agonists is tyramine, which is active at low nanomolar concentrations; the pharmacology of this response matches that of the previously published cloned insect tyramine receptor. In addition, the tubule appears capable of synthesizing tyramine from applied tyrosine, as shown by direct measurement of tyrosine decarboxylase activity. Immunohistochemical staining of tubules with an antibody against tyramine indicates that the principal cells are the sites of tyramine production, whereas previous characterization of the regulation of chloride conductance suggests that tyramine acts on the stellate cells. This is the first demonstration of a physiological role for an insect tyramine receptor.

Animals↗

PubMed1979

Tyramine kinetics and metabolism in cirrhosis.

Hypertyraminemia is common in hepatic cirrhosis and correlates in severity with encephalopathy. The mechanism of cirrhotic hypertyraminemia has not been established. The alternative possibilities are increased production from tyrosine and impaired degradation by monoamine oxidase. This investigation determined the pharmacokinetics of tyramine after an intravenous bolus injections of [3H]-tyramine (180--200 muCi 12 Ci/mmol sp act) in 13 cirrhotics and 9 controls. In normals, [3H]tyramine levels initially declined rapidly (alpha-phase) followed by a slower decline (beta-phase) with an average t 1/2 of 20.8 min. Average normal metabolic clearance rate and production rate were 13.2 liters/min and 15.4 microgram/min, respectively. In cirrhotic patients, the plasma disappearance curve for [3H]tyramine was qualitatively similar to that of the control subjects with no apparent different in beta-t 1/2 (17.2 min). The hypertyraminemia of cirrhosis resulted primarily from overproduction of tyramine, as the production rate (32.0 microgram/min) in these patients was significantly greater (P less than 0.05) than in controls, whereas the metabolic clearance rate remained normal (average 12.2 liters/min). A difference in ratio of tyramine metabolic products was noted as well. Cirrhotics had a high ratio of plasma 4-hydroxyphenylethanol:4-hydroxyphenylacetic acid (60:40 vs. 30:70) as compared with normals. Although the tyramine clearance rates are similar in normals and cirrhotics, different mechanisms may be responsible for catabolism.

Adult↗

PubMed2001

Linezolid, a novel oxazolidinone antibiotic: assessment of monoamine oxidase inhibition using pressor response to oral tyramine.

The primary objective of this study was to compare the effects of oral linezolid with moclobemide and placebo on the pressor response to oral tyramine. Secondary objectives were to determine possible mechanisms of the effect based on changes in the pharmacokinetics of tyramine and to evaluate alternative methods for quantifying the pressor effect. Subjects received linezolid (625 mg bid orally), moclobemide (150 mg tid orally), or placebo for up to 7 days. Using the oral tyramine dose producing a >30 mmHg increase in systolic blood pressure (SBP) (PD>30), a positive pressor response was defined as a PD>30 index (pretreatment/treatment ratio of PD>30) of > or = 2. There were 8/10, 11/11, and 1/10 responders with linezolid, moclobemide, and placebo, respectively. Responses returned to baseline within 2 days of drug discontinuation. The ratio of mean greatest SBP and heart rate at the time of greatest SBP (GSBP/HR) increased linearly with tyramine dose both pretreatment and during treatment with linezolid and moclobemide. During treatment, responses to tyramine when subjects took linezolid or moclobemide were significantly different from placebo. Both drugs significantly decreased tyramine oral clearance compared with placebo. Urinary excretion of catecholamines and metabolites was consistent with MAOI activity of the drugs, but results were variable. The MAOI activity of linezolid is similar to that of moclobemide, a drug used clinically without food restrictions. Restrictions to normal dietary intake of tyramine-containing foods are not warranted when taking linezolid.

Acetamides↗

PubMed1985

p-Tyramine, a natural amine, inhibits prolactin release in vivo.

p-Tyramine, an endogenous amine with sympathomimetic action, is found in the mammalian hypothalamus. When injected ip, p-tyramine reduced serum PRL without altering LH and TSH serum titers in adult orchidectomized rats and rats subjected to ether or immobilization stress. The hyperprolactinemia achieved by this last procedure was inhibited by both tyramine and dopamine; tyramine produced the same effect as dopamine at a dose 5 times greater. When PRL levels were increased by pretreatment with alpha-methyl-p-tyrosine or haloperidol, once again both tyramine and dopamine lowered PRL titers. The hypoprolactinemic effect of p-tyramine was also observed in median eminence-lesioned animals, suggesting a pituitary site of action. These results show that low amounts of tyramine, a naturally occurring amine, can inhibit in vivo increases in PRL levels achieved physiologically or pharmacologically.

Animals↗

PubMed1982

Responses of isolated dog coronary arteries to tyramine.

In isolated dog coronary arteries contracted with prostaglandin F2 alpha, tyramine in concentrations of 10(-6) and 5 x 10(-6) M caused relaxations, but it produced contractions at 2 x 10(-5) M or higher. The relaxant response to tyramine was attenuated, but the contractile response was enhanced at the second trial as compared with the responses at the first. Relaxations induced by low concentrations of tyramine were reversed to contractions by treatment with propranolol (10(-6) M) or sotalol (10(-5) M), and were abolished by cocaine (3 x 10(-6) M) or bretylium (2 x 10(-5) M). In coronary arteries isolated from reserpine (0.5 mg/kg)-pretreated dogs, tyramine produced only a contraction. Under resting conditions, contractions induced by tyramine (5 x 10(-6) to 2 x 10(-3) M) were potentiated by cocaine and propranolol, and were inhibited by phentolamine. Norepinephrine produced a dose-dependent relaxation in the arteries contracted with prostaglandin F2 alpha. In the presence of propranolol, the arteries under resting conditions were contracted by norepinephrine, the contraction being suppressed by treatment with phentolamine. It may be concluded that relaxations of dog coronary arteries induced by tyramine are mediated by liberation of norepinephrine from adrenergic nerves which stimulates beta-adrenoceptors in the smooth muscle. It seems likely that the tyramine (2 x 10(-5) M or higher)-induced contraction is not mediated by norepinephrine released, but it is partly due to a direct action on alpha-adrenoceptors.

Animals↗

PubMed1999

Refining the MAOI diet: tyramine content of pizzas and soy products.

BACKGROUND: Continuous refinement of the monoamine oxidase inhibitor (MAOI) diet has resulted in much reduced and simplified recommendations that attempt to balance safety and practicality. In the spirit of evidence-based practice, dietary restrictions should be based on carefully documented case reports and valid tyramine analyses. Residual concerns have focused on combination foods such as pizza and a variety of soy products. We determined the tyramine content of pizzas and a variety of soy products in order to refine dietary recommendations for use with MAOIs. METHOD: High-pressure liquid chromatography analysis of tyramine content was performed on a variety of pizzas, soy sauces, and other soybean products. A tyramine level of 6 mg or less was considered safe. RESULTS: No significant tyramine levels were found in any of the pizzas, including those with double pepperoni and double cheese. Marked variability was found in soy products, including clinically significant tyramine levels in tofu when stored for a week and high tyramine content in one of the soy sauces. CONCLUSION: Pizzas from large chain commercial outlets are safe for consumption with MAOIs. However, caution must be exercised if ordering pizzas from smaller outlets or gourmet pizzas known to contain aged cheeses. All soybean products should be avoided, especially soy sauce and tofu. Individualized counseling and continuous surveillance of compliance are still essential.

Acute Disease↗

PubMed2000

Tyramine injections reduce locust viability.

In the locust nervous system, tyramine is the direct precursor for octopamine synthesis and, as an octopamine analogue, it can activate octopamine receptors. Furthermore, the identification of specific tyramine receptors in Locusta migratoria and Drosophila melanogaster suggests that it is an important transmitter or modulator candidate. In this paper, we report that repeated tyramine injections reduced the viability of last instar larvae of Locusta and Schistocerca. In addition, a retardation of the last ecdysis was observed as a sublethal effect of the repeated tyramine treatment. Moreover, egg deposition by adult females was also retarded and/or drastically reduced. These effects show similarity to sublethal effects described for certain "insecticidal" octopamine receptor agonists, such as formamidines and phenyliminoimidazolidines. Since certain formamidine compounds were also shown to be agonists for the cloned tyramine receptors, it cannot be excluded that some lethal or sublethal consequences of tyramine administration are the result of an interaction with specific tyramine receptors.

Animals↗

PubMed1992

Dietary sodium restriction and pressor responsiveness to tyramine in spontaneously hypertensive rats.

OBJECTIVE: To determine in vivo whether in young spontaneously hypertensive rats (SHR) dietary sodium restriction decreases adrenergic transmitter release from the sympathetic nerve terminal. DESIGN: Dietary sodium restriction was initiated in young and mature SHR and Wistar-Kyoto (WKY) rats, and subsequently changes in pressor responsiveness to norepinephrine and to the indirectly acting sympathomimetic tyramine were determined in relation to their effects upon plasma catecholamines. RESULTS: In young SHR sodium restriction for 3-6 weeks prevented the development of hypertension, whereas in mature SHR sodium restriction did not affect blood pressure. Sodium restriction caused modest decreases in pressor responsiveness to the exogenous alpha-agonist, not different in young and mature SHR compared with WKY rats. In contrast, sodium restriction markedly inhibited pressor-responses to tyramine in young SHR and WKY rats, but not at all in mature rats. Tyramine increased plasma norepinephrine 5-10-fold. However, sodium restriction did not affect this response. The pressor response to tyramine was related to increases in total peripheral resistance, with minimal changes in cardiac output, and could be blocked by alpha 1-receptor blockade in rats on either control or low-sodium diets. CONCLUSIONS: These results show that sodium restriction causes only a small decrease in the pressor response to norepinephrine, but a more marked inhibition of the pressor response to tyramine in young SHR and WKY rats without affecting the plasma norepinephrine response to tyramine. These results suggest that dietary sodium can indeed affect presynaptic functions in vivo, but that plasma norepinephrine responses to tyramine may not reflect changes in arterial norepinephrine release, or that sodium restriction affects a co-transmitter rather than norepinephrine release per se.

Animals↗

PubMed1990

Tyramine-O-sulfate, in addition to tyrosine-O-sulfate, is produced and secreted by HepG2 human hepatoma cells, but not by 3Y1 rat embryo fibroblasts.

The spent media of HepG2 human hepatoma cells and 3Y1 rat embryo fibroblasts labeled with [35S]sulfate, upon ultrafiltration, were analyzed by a two-dimensional thin-layer separation procedure. Autoradiographs of the cellulose thin-layer plate revealed the presence of tyramine-O-[35S]sulfate in addition to tyrosine-O-[35S]sulfate in spent medium from human hepatoma cells. In contrast, only tyrosine-O-[35S]sulfate was observed in spent medium of 3Y1 rat fibroblasts. Using adenosine, 3'-phosphate, 5'-phospho[35S]sulfate as the sulfate donor, sulfotransferase(s) present in HepG2 cell homogenate catalyzed the sulfation of tyramine to tyramine-O-[35S]sulfate, but not the sulfation of tyrosine to tyrosine-O-[35S]sulfate. Endogenous aromatic amino acid decarboxylase present in HepG2 homogenate was shown to catalyze the decarboxylation of [3H]tyrosine to form [3H]tyramine while attempts to use it for the decarboxylation of tyrosine-O-sulfate to form tyramine-O-sulfate were unsuccessful. These results suggest that tyramine-O-sulfate may be derived from the de novo sulfation of tyramine, instead of the decarboxylation of tyrosine-O-sulfate.

Animals↗

PubMed2006

Effects of tyramine administration in Parkinson's disease patients treated with selective MAO-B inhibitor rasagiline.

Rasagiline is a novel, potent, and selective MAO-B inhibitor shown to be effective for Parkinson's disease. Traditional nonselective MAO inhibitors have been associated with dietary tyramine interactions that can induce hypertensive reactions. To test safety, tyramine challenges (50-75 mg) were performed in 72 rasagiline-treated and 38 placebo-treated Parkinson's disease (PD) patients at the end of two double-blind placebo-controlled trials of rasagiline. An abnormal pressor response was prespecified as three consecutive measurements of systolic blood pressure (BP) increases of >or= 30 mm Hg and/or bradycardia of < 40 beats/min. In the first study involving 55 patients with early PD on rasagiline monotherapy, no patients randomized to rasagiline (1 mg/2 mg; n = 38) or placebo (n = 17) developed systolic BP (SBP) or heart rate changes indicative of a tyramine reaction. In the second trial involving 55 levodopa-treated patients, 3 of 22 subjects on rasagiline 0.5 mg/day and 1 of 21 subjects on placebo developed asymptomatic, self-limiting SBP elevations >or= 30 mm Hg on three measurements. No subject on 1 mg/day rasagiline (0/12) experienced significant BP or heart rate changes following tyramine ingestion. These data demonstrate that rasagiline 0.5 to 2 mg daily is not associated with clinically significant tyramine reactions and can be used as monotherapy or adjunct to levodopa in PD patients without specific dietary tyramine restriction.

Administration, Oral↗

PubMed1963

Interactions between cocaine, tyramine and noradrenaline at the noradrenaline store.

In the cat, the pressor actions of noradrenaline and of adrenaline were generally reduced and that of tyramine was increased during infusions either of noradrenaline or of adrenaline. The increase in the response to tyramine after an infusion of noradrenaline was prevented by cocaine, methyl phenidate and pipradrol. Pipradrol, unlike its isomer azacyclonol, increased the responses to catechol amines but reduced that to tyramine. Cocaine did not prevent the increase in the noradrenaline content of cat kidney and uterus after an infusion of noradrenaline. In the pithed rat, cocaine increased the pressor response to noradrenaline but antagonized that to tyramine. Treatment of the rat with reserpine prevented the effect of cocaine on the response to tyramine but did not modify the potentiation of the response to noradrenaline. Prolonged treatment with cocaine did not lower the tissue noradrenaline levels and did not prevent the noradrenaline depletion by reserpine. It is suggested that interactions between cocaine, tyramine and noradrenaline occur at the point where noradrenaline enters its tissue store.

Amines↗

PubMed1963

THE RESPONSES TO TYRAMINE OF THE NORMAL AND DENERVATED NICTITATING MEMBRANE OF THE CAT: ANALYSIS OF THE MECHANISMS AND SITES OF ACTION.

The response to tyramine of the denervated nictitating membrane has been analysed by comparing dose/response curves obtained by injections into the femoral vein and into the carotid artery of the spinal cat while recording contractions of innervated and chronically denervated membranes and those of cats treated with reserpine. It is concluded that the effect of tyramine given by these routes is due primarily to catechol amines released from stores within the nictitating membrane itself. Higher doses of tyramine also cause contraction of the membrane by liberating catechol amines into the circulating blood from stores outside the membrane. The response to tyramine of the nictitating membrane after chronic denervation and/or prior treatment with reserpine is partially due to catechol amines released from unidentified stores within the membrane which resist depletion by reserpine and by postganglionic denervation; evidence is presented that adrenaline rather than noradrenaline is concerned. Because of the high sensitivity of the denervated nictitating membrane to adrenaline and to noradrenaline, the response to these amines released from stores outside the membrane by intravenous injections of tyramine becomes greater than that of the normal membrane. Dose/response curves obtained from responses to intravenous sympathomimetic drugs which act away from the membrane are therefore not fully representative of the effect of the drugs on the membrane itself. Tyramine probably has an affinity both for storage sites and for catechol amine receptors in the smooth muscle of the nictitating membrane, the "intrinsic activity," however, being very weak or even absent.

Amines↗