PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “PHENYLETHYLAMINES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 145 records · Page 8Linked to original sources
PubMed1995

Characterization of the vasorelaxant activity of tyramine and other phenylethylamines in rat aorta.

We recently reported that tyramine caused concentration-dependent relaxation of rat aorta, which was endothelium independent and was not exerted via alpha 1-adrenoceptors (AR), alpha 2AR, beta 1AR, beta 2AR, or receptors for 5-hydroxytryptamine, histamine, and adenosine. The present studies were done on endothelium-denuded strips to determine structure-vasorelaxant activity after blockade of beta AR by propranolol plus irreversible blockade of alpha 1AR with benextramine. Vasorelaxation under these conditions was limited to noncatecholamines, and their vasorelaxant potencies were methoxyphenamine > tyramine > p-hydroxyephedrine > L-amphetamine > L-ephedrine > phenylethylamine > synephrine > methoxamine > octopamine. beta 3AR agonists (BRL 37344 and CGP 12177A) did not produce vasorelaxation, although tyramine could compete for cyanopindolol binding to murine L cells expressing human beta 2AR or beta 3AR. There was no significant specific binding of [3H]tyramine to aortic membrane preparations after the inhibition of monamine oxidase. Yohimbine, which has a high affinity for Drosophila tyramine receptors, also caused dose-dependent vasorelaxation like tyramine. It is concluded that tyramine and several other phenylethylamines produce relaxation of rat aorta, which does not involve any of the known adrenoceptors but may be exerted via novel tyramine receptors.

Animals↗
PubMed1975

[Central action of beta-phenylethylamine derivatives. (4) Effects on spontaneous motor activity and body temperature of beta phenylethyamine derivatives injected into the brain in reserpine pretreated mice].

Effects on spontaneous motor activity and body temperature of beta-phenylethlamine derivatives injected into the cerebral ventricles in reserpine or reserpine and isocarboxazide pretreated mice were investigated with the following results. 1) Each injection of tyramine (40 mug) and dopamine (40 mug) increased the spontaneous motor activity measured by the photo-cell counters method in reserpinized mice. 2) Each injection of tyramine (40 mug), dopamine (40 mug) and beta-phenylethylamine (40 mug) increased the spontaneous motor activity measured by both the wheel cage and photo-cell counters methods in reserpine and isocarboxazide-pretreated mice, but noradrenaline (20 mug) and isoproterenol (80 mug) did not increase the spontaneous motor activity as determined by both methods. 3) The injection of tyramine (40 and 80 mug), dopamine (10 and 40 mug) and p-octopamine (40 mug) increased the body temperature in reserpine and isocarboxazide pretreated mice. 4) Tyramine, dopamine and p-octopamine caused a marked increase in the body temperature as compared with control injection in reserpine and isocarboxazide-pretreated mice, whereas isoproterenol had no influence on body temperature. Our results suggest that beta-phenylethylamine derivatives have different effects in reserpinized and non-pretreated states.

Animals↗
PubMed1993

Characteristics of antinociception induced by noncatecholic phenylethylamine derivatives: the involvement of alpha-2-adrenoceptors.

Characteristics of the antinociceptive action of phenylethylamine derivatives, amphetamine, beta-phenylethylamine (PEA) and beta-hydroxyphenylethylamine (OHPEA), were examined. The antinociception induced by PEA derivatives was enhanced by intracisternal injection of norepinephrine or clonidine and attenuated by intracisternal injection of phentolamine or yohimbine, but was not affected by intracisternal injection of prazosin in the mouse hot plate method. PEA derivatives induced a contraction of the rat vas deferens, and this contraction by PEA derivatives was attenuated by the application of phentolamine. The contractions induced by PEA or OHPEA in the reserpinized vas deferens were much smaller than those in the normal one. PEA derivatives inhibited the electrical stimulation-evoked contractions of the vas deferens, and the inhibition by PEA derivatives was reversed by the application of yohimbine. These findings indicate that PEA derivatives may induce the antinociception as a result of stimulating the alpha 2-adrenoceptors. The stimulation of alpha 2-adrenoceptors by PEA derivatives may result from the release of endogenous norepinephrine and/or from direct action on the alpha 2-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed2002

Spectroscopic evidence in support of horseradish peroxidase compound II-catalyzed oxidation of salicylic acid but not of phenylethylamine.

Salicylic acid and phenylethylamine are putative substrates for naturally occurring reactions for generation of reactive oxygen species, which are catalyzed by plant peroxidases. Here, we used commercially available highly purified horseradish peroxidase-C (HRP-C) as a model enzyme for spectroscopic analysis, and obtained data suggesting that the Compound II form of HRP-C does not utilize phenylethylamine as substrate. In contrast, addition of salicylic acid to Compound II resulted in rapid conversion of Compound II to the native form.

Catalysis↗
PubMed1999

Production of 2-phenylethylamine by decarboxylation of L-phenylalanine in alkaliphilic Bacillus cohnii.

Cellular polyamine fraction of alkaliphilic Bacillus species was analyzed by HPLC. 2-Phenylethylamine was found selectively and ubiquitously in the five strains belonging to Bacillus cohnii within 27 alkaliphilic Bacillus strains. A large amount of this aromatic amine was produced by the decarboxylation of L-phenylalanine in the bacteria and secreted into the culture medium. The production of 2-phenylethylamine may serve for the chemotaxonomy of alkaliphilic Bacillus.

Journal Article↗
PubMed1981

Toxicological analysis of phenylethylamines by high performance reversed-phase ion-pair partition thin-layer and liquid chromatographies.

A rapid and specific method was developed to identify phenylethylamines in urine. After an organic extraction at appropriate pH, reverse phase ion-pair partition chromatographies were used: a high performance thin-layer test followed by high performance liquid chromatography. The use and benefits of the procedure are described in detail and compared with other methods. In a very short time (10 min) the presence of phenylethylamine is detected on a thin-layer plate. In the case of positive result the product is then specifically identified by high performance liquid chromatography by means of a complete UV spectrum traced directly on the eluated compound. The sensitivity of the method is highly increased because the detection is operated at 215 nm.

Chromatography, High Pressure Liquid↗
PubMed1975

Beta-phenylethylamine and locomotor activity in mice. Interaction with catecholaminergic neurones and receptors.

Beta-Phenylethylamine on injection into mice produced both an early and late phase of increased locomotor activity. The early phase produced by 50 mg phenylethylamine/kg was inhibited by pretreatment with phenoxybenzamine, phentolamine, alpha-methyl-tyrosine, diethyldithiocarbamate, pimozide and haloperidol, but not by propranolol, protriptyline and reserpine. The late phase produced by 100 mg phenylethylamine/kg was blocked only by pimozide and haloperidol, both of these in doses at least ten times higher than those required to block the early phase. From these results it was concluded that the increased early phase of locomotor activity was due to the release of dopamine and noradrenaline synthetic pathway, but not intact reserpine sensitive amine stores. In contrast the late phase of locomotor activity was independent of catecholamine stores and appeared to be produced by a direct action by either phenylethylamine or metabolites on dopamine receptors.

Animals↗
PubMedDate not supplied

[The anxiogenic activity of phenylethylamine in the social isolation test on mice].

One-day isolation of male albino mice of SHR strain significantly increased the level of social behaviour measured by the number and total duration of active contacts (sniffings). A putative endogenous anxiogen beta-phenylethylamine (5-12.5 mg/kg) inhibited the communication like human anxiogens corazole (10 mg/kg) and caffeine (200 mg/kg). Diazepam (1 mg/kg) prevented the action of phenylethylamine, phenibut (10-50 mg/kg) exerted no effect on it. The social isolation test during studying anxiogens and anxiolytics can be performed on mice as previously on rats.

Animals↗
PubMed1978

Testosterone-attenuated stereotype and hyperactivity induced by beta-phenylethylamine in pargyline-pretreated rats.

Testosterone pretreatment (1.0-4.0 mg/kg) attenuated, in a dose-response fashion, the induction of stereotyped behavior and hyperactivity by pargyline (0.25, 4.0 mg/kg) and beta-phenylethylamine (8.0, 16.0 mg/kg) in preubertal, male rats. The dyskinetic movements induced by pargyline and beta-phenylethylamine were proposed as a possible animal model for tardive dyskinesias. Attenuation by testosterone of these effects suggested an hormonal involvement consistent with the reported predominant occurrence of tardive dyskinesias in women and in the elderly.

Animals↗
PubMedDate not supplied

Cytochrome P-455-nm complex formation in the metabolism of phenylalkylamines. VI. Structure--activity relationships in metabolic intermediary complex formation with a series of alpha-substituted 2-phenylethylamines and corresponding N-hydroxylamines.

The formation of cytochrome P-450 metabolic intermediary (MI) complexes from a homologous series of alpha-substituted 2-phenylethylamines and corresponding N-hydroxylamines was investigated during NADPH-dependent metabolism in liver microsomes from phenobarbital-pretreated rats. The alpha-alkyl substituent consisted of branched and unbranched alkyl chains ranging from 0-4 carbons and the benzyl group. All the compounds but 2-phenylethylamine generated the complex and double-reciprocal plots of the highest observed rate of complex formation vs. substrate concentration gave linear relations over a defined substrate range. The Vmax(obs) values for complex formation by the amines increased markedly with increasing size of the alkyl group and a good correlation was obtained between log Vmax(obs) and the logarithm of the octanol/buffer partition coefficient of the substrates. With the N-hydroxy compounds, complex formation was a much less selective phenomenon and without exception the rates were quite high with Vmax(obs) values as much as 100 times greater than those of the amines. The disappearance of substrate amines was independent of structure and at an initial substrate concentration of 100 microM about a 50% decrease was noted during a 20-min period in all cases. The results substantiate the previous notion that N-oxidation is a prerequisite for MI-complex formation from primary amines. The results also suggest that C- and N-oxidation have different rate-limiting steps and the microsomal enzymes catalyzing the N-oxidation seem to be deeply submerged in the lipid matrix, as amines with a low distribution are inactive or poor substrates for generating the cytochrome P-450 ligand. Also, it is evident that the MI complex formation does not impair the overall metabolism of the amines.

Animals↗
PubMed1978

Evidence for the presence of m-tyramine, p-tyramine, tryptamine, and phenylethylamine in the rat brain and several areas of the human brain.

Postmortem human brains have been obtained from four nonpsychiatric patients, aged 59-70 years. Regional analysis of the trace amines phenylethylamine, p-tyramine, m-tyramine, and tryptamine has indicated that the amines are distributed heterogeneously throughout the brain, but are most concentrated in the basal ganglia. Although the levels are very low, evidence obtained from animal studies has indicated that the trace amines have a very rapid turnover rate. Their presence in a brain synaptosomal fraction suggests a possible involvement in the process of neurotransmission. Postmortem changes in human brain amines are discussed in relation to those occurring postmortem in the rat brain, in which phenylethylamine, p-tyramine, and tryptamine have been shown to increase to levels greater than those prevailing in vivo.

Aged↗
PubMed1984

Behavior maintained under fixed-interval and second-order schedules by intravenous injections of endogenous noncatecholic phenylethylamines in dogs.

The effectiveness of i.v. injections of the endogenously occurring amines beta-phenylethylamine (PEA), N-methyl phenylethylamine (NMPEA) and phenylethanolamine in maintaining schedule-controlled behavior was investigated in dogs. Behavior was maintained under either a fixed-interval (FI) 5-min schedule of i.v. drug injection or a second-order FI 5-min schedule where every fifth response (FR 5) resulted in a 2-sec visual stimulus and the first FR 5 completed after the interval elapsed resulted in both the visual stimulus and i.v. drug injection [FI 5-min (FR 5:S)]. Experimental sessions, with 10 intervals per session, were conducted 5 days/week. Each drug injection was followed by a 5-min timeout period to minimize the direct effects of the drugs on responding. As the dose per injection increased, rates of responding maintained under both schedules by PEA and NMPEA first increased and then decreased. When saline was substituted for drug, responding occurred at very low rates. PEA and NMPEA were approximately equieffective and equipotent in maintaining responding under the FI 5-min schedule. PEA maintained somewhat higher rates under the FI 5-min (FR 5:S) schedule; rates maintained by NMPEA under the second-order schedule were comparable to those maintained under the simple FI schedule. Phenylethanolamine failed to consistently maintain responding under either schedule. Injections of PEA and NMPEA controlled overall patterns of positively accelerated responding under both schedules, whereas the local pattern of responding under the second-order schedule was under the control of both the brief stimulus presentations as well as drug delivery.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Endothelium- and beta-2 adrenoceptor-independent relaxation of rat aorta by tyramine and certain other phenylethylamines.

At concentrations higher than that required to produce maximal vasoconstriction, tyramine caused concentration-dependent relaxation of rat aortic strips contracted maximally by tyramine, norepinephrine, phenylephrine, 5-hydroxytryptamine, prostaglandin F2 alpha, endothelin, angiotensin II and potassium; isoproterenol did not relax potassium-contracted strips. The vasorelaxant effect of tyramine was not antagonized by propranolol, pindolol or nadolol, all of which markedly antagonized the effects of isoproterenol. The vasorelaxant activity of tyramine was endothelium-independent and not inhibited by hemoglobin, methylene blue or L-NG-nitro arginine; it did not exhibit tachyphylaxis and was neither inhibited by cocaine, guanethidine, reserpine and chemical sympathectomy nor by alpha adrenoceptor, dopamine receptor, 5-hydroxytryptamine receptor, histamine receptor and adenosine receptor antagonists. Inhibition of cyclooxygenase, lipoxygenase and monamine oxidase activities did not decrease the vasorelaxant activity of tyramine. The vasorelaxant effect of tyramine was not decreased by altering external calcium from 0.25 to 4 mM nor was it potentiated by nifedipine. Phenylethylamine was the minimum structural requirement for this propranolol-resistant vasorelaxant activity; beta-carbon and 3-ring hydroxylation abolished this activity, but N-methylation partly overcame the effect of beta-hydroxylation. The vasopressor effect of tyramine in anesthetized rat was reversed to vasodepressor effect by phenoxybenzamine plus propranolol. The propranolol-resistant vasorelaxant effect of tyramine was also confirmed on isolated human placenta arteries. At vasorelaxant concentrations, tyramine did not increase cyclic GMP and cyclic AMP but inhibited inositol-1,4,5-triphosphate. It is suggested that at high concentrations tyramine and related phenylethylamines cause endothelium- and beta-2 adrenoceptor independent vasorelaxation either via specific tyramine receptors or nonselectively.

Animals↗
PubMed2001

Investigation of the physicochemical basis of enantiomeric enrichment: The example of alpha-phenylethylamine with achiral dicarboxylic acids.

We investigated the enantiomeric enrichment of enantiomeric mixtures of alpha-phenylethylamine by achiral dicarboxylic acids. As achiral agents oxalic, malonic, fumaric, and phthalic acids were used. The results of the enantiomeric enrichment via partial salt formation followed by distillation were compared with enantiomer separation via crystallization of the neutral salt. Without the presence of a solid phase, enantiomeric separation is impossible. Our results show that the properties of the solid phase determine the separation. It is also confirmed by our observation that the eutectic points, which are observed on the 3-phase solubility diagrams of the solid neutral salts, can be found at the same initial enantiomeric composition as the point of intersection of distillate and residue of the distillation curves and the point of intersection of precipitated salt and mother liquor of the crystallization curves. Copyright 2000 Wiley-Liss, Inc.

Journal Article↗
PubMed2005

Responses of the silkworm tyramine receptor to 2-phenylethylamines and 5-phenyloxazoles.

Tyramine (TA), a biogenic amine, attenuates intracellular cAMP production by acting on its receptor in insects. Several non-biogenic amines were examined for their actions on native and heterologously expressed silkworm TA receptors. 5-(4-Hydroxyphenyl)oxazole, which showed an attenuating effect on cAMP production in silkworm-head membranes, did not attenuate forskolin-stimulated cAMP production in HEK-293 cells expressing the silkworm TA receptor, although the compound bound to the cloned receptor. 2-Phenylethylamines (2-PEAs), which showed positive and negative effects on cAMP production in silkworm-head membranes, inhibited [3H]TA binding to the cloned TA receptor. 2-Chloro-2-(4-chlorophenyl)ethylamine was the most potent inhibitor of [3H]TA binding among the 2-PEAs tested, with an IC50 of 30.4 nM. This compound acted as an antagonist and abolished TA-attenuation of forskolin-stimulated cAMP production in the cloned TA receptor. The discrepancy in the effects of the non-biogenic amines on the native and cloned TA receptors remains to be further examined. A newly synthesized 2-PEA, 2-chloro-2-(4-hydroxyphenyl)ethylamine, attenuated forskolin-stimulated cAMP production in the cloned TA receptor, indicating that the para-hydroxy group is important for the agonist action.

Animals↗
PubMed1994

Role of conductivity in iontophoresis. 2. Anodal iontophoretic transport of phenylethylamine and sodium across excised human skin.

The anodal iontophoretic transdermal delivery of a model cation, phenylethylamine (PEA), across excised human skin was investigated to define the role of conductivity in iontophoresis. The ratio of the specific conductance of PEA in deionized-distilled water to that of the solution applied in the donor compartment (buffer+PEA) was employed to assess the relationship between the flux of PEA and the conductivity. The flux of PEA was linearly related to the ratio of specific conductance at 5 and 20 mM PEA for a variety of experimental conditions. A curvilinear relationship was observed at 1 mM PEA concentration, particularly when the conductivity of the donor solution was low. It is therefore hypothesized that a threshold conductivity in solution exists above which a linear relationship between iontophoretic flux and specific conductance is observed. The present study confirms that conductivity of an ion in a solution provides a simple means of estimating the competitive transport between solute and other ions during transdermal iontophoresis.

Buffers↗
PubMed1992

The determination of low d5-phenylalanine enrichment (0.002-0.09 atom percent excess), after conversion to phenylethylamine, in relation to protein turnover studies by gas chromatography/electron ionization mass spectrometry.

A gas chromatography/mass spectrometry (GC/MS) method for measuring very low levels of enrichment of d5-phenylalanine (0.002-0.09 atom percent excess) is described. This method makes it possible to determine the enrichment of amino acid incorporated into tissue protein during studies of protein synthesis in man. Phenylalanine is enzymatically converted to phenylethylamine and the d5-enrichment is measured in the heptafluorobutyryl derivative by selective-ion recording under electron ionization conditions. The coefficients of variation for muscle-protein hydrolysate samples enriched with d5-phenylalanine at the 0.005 and 0.05 atom percent excess levels were 6.0 and 1.2%, respectively. This precision at low enrichment and the small amount of protein needed (about 1 mg) provide real advantages for clinical studies of tissue protein synthesis. Moreover, in contrast to the conventional approach which uses GC/MS for plasma amino acids (typically 2-20 atom percent excess) but gas isotope-ratio mass spectrometry for protein-bound amino acids, the enrichment of both plasma-free and protein-bound d5-phenylalanine can be measured with a single instrument.

Gas Chromatography-Mass Spectrometry↗