Disease relevance of p-Tyramine

• Thus the effects of p-tyramine with or without a monoamine-oxidase inhibitor were unpredictable and did not include relief of postural hypotension [1].
• In supine patients p-tyramine alone or with a monoamine-oxidase inhibitor produced pronounced supine hypertension without abolishing the symptoms associated with a postural fall in blood-pressure [1].
• 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 [2].
• 4. The possibility of the patient with hereditary tyrosinemia providing a model to study the origin of urinary p-tyramine is discussed [3].

Psychiatry related information on p-Tyramine

• In males, weak but significant linear correlations (Pearson product-moment and Spearman rank correlations) were found between platelet MAO activity (p-tyramine and benzylamine as substrates) and the extraversion/introversion dimension [4].
• The possible existence of a direct receptor-stimulating activity of p-tyramine was examined by injecting this amine intraventricularly into rats, after pretreatment with various drugs, which inhibit catecholaminergic function, and measuring their motor activity [5].
• The value of MAO activity measurements as a means for distinguishing sub-types of schizophrenic disorders is improved by using two substrates; tryptamine and p-tyramine [6].
• With p-tyramine, MAO was low in patients with affective psychoses and paranoid schizophrenia [6].

High impact information on p-Tyramine

• The relative bioavailability of p-tyramine after treatment was not significantly different from before treatment, although a tendency to a greater bioavailability was seen with the 12 and 24 mg doses [7].
• The presence of the so-called trace amines 2-phenylethylamine, m-tyramine, p-tyramine, m-octopamine, p-octopamine and tryptamine in the mammalian central nervous system has been known for several decades [8].
• Whereas the spectral binding affinity for 3-methoxyphenethylamine and 4-methoxyphenethylamine was similar, the affinity for 4-hydroxyphenethylamine was 12-fold weaker than for 3-hydroxyphenethylamine at pH 7 [9].
• Unlike catecholamines, there is a drastic decrease of p-octopamine after 20 months of age in the hypothalamus and telencephalon. p-Tyramine levels are also lowered [10].
• P-Tyramine inhibited PRL release from hemipituitaries incubated in vitro at doses of 10(-4) and 10(-6) M (inhibition to 31% and 59% of control values, respectively) [11].

Chemical compound and disease context of p-Tyramine

• Urinary p-tyramine in hereditary tyrosinemia: I. Levels as compared to normal individuals, effect of diet, and relationship to urinary tyrosine [3].

Biological context of p-Tyramine

• Salivation in response to p-tyramine injected i.v. and i.p. was completely abolished by simultaneous injections of both prazosin and propranolol [12].
• The molecular targets for trace amines (TAs) such as p-tyramine and beta-phenylethylamine have been recently discovered and have been shown to comprise a family of G-protein-coupled receptors based on DNA sequence homologies [13].
• Uptake of [3H]DA (0.1 microM) into rat striatal synaptosomes was inhibited in a concentration-dependent manner in the following apparent rank-order: p-tyramine, N-methyl-5-HT, tryptamine, 5-HT, N-methyltryptamine (IC50 = 44-718 nM), other indoles (IC50 = 10-100 microM) [14].
• The hydroxylation of p-tyramine in man [15].
• 3. Both intestinal bacterial activity and tissue decarboxylation appeared to account for urinary p-tyramine in this patient following an oral load of tyrosine [16].

Anatomical context of p-Tyramine

• p-Tyramine, an endogenous amine with sympathomimetic action, is found in the mammalian hypothalamus [17].
• Thus, p-tyramine may activate both the alpha 1- and beta 1-adrenoceptors in the submandibular glands of rats directly or indirectly [12].
• Pre- and postsynaptic effects of p-tyramine and p-octopamine in the prostatic portion of the rat vas deferens [18].
• The N-acetylated metabolites of p-tyramine, p-octopamine and dopamine were identified unambiguously and quantitatively determined in a single ventral thoracic nerve cord of the locust, Schistocerca gregaria, by gas chromatography-negative-ion chemical ionisation mass spectrometry (GC-NICIMS) [19].
• The highest concentrations of p-tyramine were measured in the olfactory tubercle followed by the nucleus accumbens and septal nuclei while for m-tyramine the concentrations decreased in the following order: olfactory tubercle, nucleus accumbens, amygdala, septal nuclei and nucleus tractus diagonalis [20].

Associations of p-Tyramine with other chemical compounds

• Thus, we report that p-tyrosine is decarboxylated by aromatic L-amino acid decarboxylase and that this metabolic transformation may be an important source of p-tyramine in mammalian tissues [21].
• In the present experiments the action of p-tyramine on PRL release in vitro, or after challenge with different hyperprolactinemic drugs (serotonin, morphine, and TRH) was tested [11].
• The concentration of p-tyramine in the rat striatum was increased significantly by intraperitoneal injection of phenelzine (5 or 100 mg/kg) [22].
• With regard to the hypoprolactinemic potencies in the immobilization stress model, it was observed that p-tyramine, another trace amine, was as potent as octopamine [23].
• Using reversed-phase high-performance liquid chromatography and electrochemical detection with a rapid one-step purification on a Sephadex G-10 column, we have developed a sensitive technique to measure p-hydroxyphenylacetic acid, the oxidatively deaminated metabolite of p-tyramine [24].

Gene context of p-Tyramine

• The finding that the administration of an aromatic-L-amino acid decarboxylase inhibitor leads to a decrease of p-tyramine gives further evidence that this amine is synthesized from p-tyrosine, which is also found in high concentrations in the lobster nerve cord [25].
• DA, Hill coefficient 1.0, and its analogs 3-hydroxyphenethylamine and 4-hydroxyphenethylamine attenuated the effects of PG on the DAT while phenethylamine did not [26].
• 2. Urinary excretion of conjugated p-tyramine was not significantly different between normal, melancholic and non-melancholic depressed subjects [27].
• The IC50 values for all the other compounds were in the micromolar range and were different at the two binding sites except for p-tyramine (IC50, 5-HT1 = IC50, 5-HT2 = 17 microM [28].
• PPA can also inhibit MAO-A activity in vivo at relatively high dose (50 mg/kg, i.p.), which was determined from an observation that PPA can protect MAO from the irreversible MAO inhibitor clorgyline. p-Tyramine levels were found to be increased in the urine after i.p. administration of PPA [29].

Analytical, diagnostic and therapeutic context of p-Tyramine

• Normalized p-tyramine for area under the plasma concentration-time curve after treatment were not significantly different from their respective before-treatment values for any of the dose groups [7].
• 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 [17].

References