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PubMed1977

3H-metaraminol releasing action of mescaline from rat hypothalamus in vitro.

The amine releasing action of mescaline was investigated in rat isolated hypothalamus labeled with 3H-metaraminol. Mescaline had no effect on the uptake of 3H-metaraminol but produced its release in a concentration-related manner. 4 x 10(-4) M mescaline, which produced submaximal effects was used for subsequent experiments. 3 x 10(-5) M cocaine had no effect on the 3H-metaraminol releasing action of mescaline. Mescaline was fully effective in Ca2+-free medium while 6 x 10(-2) M KCl was ineffective. 3 x 10(-7) M tetrodotoxin or 6 x 10(-5) M lidocaine partially blocked mescaline-induced release but substantially or completely blocked 3 x 10(-2) M KCl-induced release. Prior exposure of hypothalamus to 3 x 10(-4) M tyramine reduced the releasing action of mescaline. Thus, mescaline appears to release 3H-metaraminol both by Ca2+-independent (tyramine-like) and Ca2+-dependent (lidocaine-sensitive) mechanisms. 3 x 10(-4) M tyramine and 6 x 10(-2) M KCl released 14C from control hypothalamus labelled with 14C-mescaline, but not from reserpinized hypothalamus. The amounts of 14C recovered in 14C-mescaline labeled control and reserpinized hypothalamus at the end of 50 min of efflux were similar suggesting a poor retention of 14C-mescaline by storage particles.

Animals↗
PubMed1978

Increases in plasma cyclic AMP dependent on endogenous catecholamines.

Administration of tyramine (with or without phentolamine) as well as induction of ether anesthesia or insulin hypoglycemia caused a sharp increase in plasma cyclic AMP in rats. Based on the findings that the treatment of rats with reserpine, 6-hydroxydopamine, cocaine or propranolol totally abolished tyramine-induced increases in plasma cyclic AMP, it was concluded that catecholamines released from sympathetic neuronal terminals by tyramine could activate adenylate cyclase via the stimulation of postsynaptic beta-adrenoceptors. In contrast, catecholamines secreted from adrenal medulla were largely responsible for the increase in plasma cyclic AMP induced by ether anesthesia; whereas glucagon, in addition to adrenal catecholamines, played a significant role in hypoglycemia-induced increases in plasma cyclic AMP. Assay of plasma cyclic AMP following these stimuli is very promising as a test for adrenergic activities in experimental and clinical studies.

Animals↗
PubMed1984

The effect of zimelidine and amitriptyline on the brain concentration of some indolic and phenolic monoamines in the mouse.

The increase in mouse brain tryptamine accumulation rate and 5-hydroxytryptamine (5-HT) concentration and the reduction in 5-hydroxyindole acetic acid concentration observed after zimelidine administration suggest that the treatment reduces the brain tryptophan availability. Amitriptyline produced no significant changes on tryptamine, 5-HT or 5-hydroxyindole acetic acid. Also, zimelidine reduced mouse brain p-tyramine, increased m-tyramine and increased homovanillic acid. Similar effects were observed after amitriptyline administration. The experiments show that both drugs affect dopamine turnover and tyramine concentration in a similar fashion to that observed for the antipsychotic group of drugs, thus suggesting that they may have some antipsychotic effects, especially if administered at the high dose levels. In addition, it may also possess some of the undesirable effects of this group of drugs.

Amitriptyline↗
PubMed1990

Biosynthesis of bisbenzylisoquinoline alkaloids in cultured roots of Stephania cepharantha.

Cultured roots of Stephania cepharantha, which are rich sources of bisbenzylisoquinoline alkaloids, were fed 14C-labelled tyrosine, tyramine or dopamine. While tyrosine was well incorporated into the bisbenzylisoquinolines, tyramine and dopamine were poorly incorporated. Incorporated tyrosine was shown to be decarboxylated and stored as tyramine in the roots, then gradually converted to the bisbenzylisoquinolines. Tracer experiments using [3-13C]tyrosine demonstrated that tyrosine was specifically incorporated into the corresponding sites of aromoline, which verified that aromoline was composed of four molecules of tyrosine. The ratio of 13C-enrichments of C-4 and C-alpha in (R) and (S) halves of aromoline was the same within experimental limits. This indicated that the two coclaurine units must have one and the same biogenetic origin.

Alkaloids↗
PubMed1982

Drug-induced release of biogenic amines from synaptosomes and blood platelets of guinea-pigs.

Synaptosomes from guinea-pig brain were compared with blood platelets (partly from previous experiments) regarding the action of imipramine, the benzoquinolizine derivative Ro 4-1284, tyramine and p-chlormethamphetamine (PCMA) on the contents of stored radio-labelled 5-hydroxytryptamine (5HT), dopamine (DA) and noradrenaline (NA). Normal and reserpinized preparations were used in order to differentiate between granular and extragranular (reserpine-resistant) sites. Imipramine, in concentrations greater than those inhibiting 5HT- and NA-uptake released the three amines from granular and extragranular sites and showed the same order of potency in synaptosomes as in platelets. The drug Ro 4-1284 acted on the granular amines only, but its action on NA was less potent in synaptosomes than in platelets. Tyramine and PCMA also caused an exclusive release of granular amines in synaptosomes, whereas in platelets the drugs released extragranular 5HT (and DA) as well as the granular amines. Tyramine was more potent in synaptosomes than in platelets, and PCMA showed a preferential effect on 5HT in synaptosomes but not in platelets. It is concluded that, regarding the action of monoamine-releasing drugs, platelets are only partial models for synaptosomes. However, they may be superior to synaptosomes in predicting the pattern of amine release in brain in vivo as seen with Ro 4-1284.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1992

Blood pressure changes and sympathetic function in rats given cyclohexylamine by intravenous infusion.

Intravenous infusion of cyclohexylamine (30-120 mg/kg) caused a dose-dependent increase in blood pressure in urethane-anesthetized rats. The increase in blood pressure was inversely related to the duration of the infusion. The blood pressure returned to baseline values (+/- 5 mm Hg) within 60 min of the end of the infusion after doses of 30 and 60 mg/kg were administered over 20 and 40 min. The plasma concentrations of cyclohexylamine were related linearly to the administered dose and decreased only 27% between the end of the infusion and 60 min later. The concentration-effect relationship showed clockwise hysteresis, indicative of tachyphylaxis, as has been reported in humans (Eichelbaum et al., 1974). Administration of bolus doses of tyramine at the end of the infusion or 60 min later demonstrated the presence of an indirect sympathomimetic response, although this was attenuated to a greater extent by high doses and more rapid infusions of cyclohexylamine. An almost complete loss of response to tyramine was found only in animals given 120 mg/kg over 40 min. The presence of a tyramine response 60 min after the infusion of 60 mg/kg occurred when there was an essentially complete reversal of the hypertensive effect of cyclohexylamine. These data indicate that the hypertensive effect of the indirectly acting sympathomimetic amine cyclohexylamine occurs primarily during rapid increases in plasma concentrations. Tachyphylaxis develops rapidly after the cessation of the infusion which is probably due largely to reuptake of released noradrenaline at low doses and depletion of releasable noradrenaline at high doses.

Animals↗
PubMed1981

Method for localized and sustained administration of drugs to the vas deferens of rats.

A simple method is described for constructing collars (15 mm long, 6.5 mm diameter with a central hole 2.8 mm diameter) consisting of powdered tyramine HCI dispersed in polydimethylsiloxane polymer (Silastic). Release rate was measured (1) by incubation at 37 degrees C in 100 ml of tris buffer at pH = 7.4 (in vitro) and (2) after fitting to the vasa deferentia of rats, by collection of their urine and analysis for p-hydroxyphenylacetic acid (in vivo). Collars containing 50% tyramine released their load over about 7 weeks both in vivo and in vitro. The rate of release was initially linear and later proportional to (time) 1/2, these kinetics being consistent with the matrix model. The useful life of these devices is about 3 weeks since this is the period of substantial daily release. The rate of release is greater when the proportion of tyramine in the tyramine/Silastic mixture is increased (useful range = 25-50%). Release is prolonge and further localized by partly coating the collar with a layer of drug-free Silastic.

Animals↗
PubMed1986

Relation of nitrite concentration to mutagen formation in soy sauce.

When soy sauce was mixed with nitrite solutions at pH 1.0 and 3.0, only mixtures containing nitrite concentrations above 250 ppm were mutagenic in the Salmonella/mammalian microsome test. In buffered aqueous solution (pH 3) the mutagen precursor, (-)-(1S,3S)-1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid [(1S,3S)-MTCA] and its stereoisomer ( - )-(1R,3S)-MTCA reacted with 10 ppm or more of sodium nitrite; but at least 250 ppm nitrite was required for them to react in soy sauce (pH 3). Similarly, another mutagen precursor, tyramine, did not react even with 2300 ppm nitrite in soy sauce (pH 1), although pure tyramine in aqueous solution (pH 1) reacted with as little as 50 ppm nitrite. Nitrite concentration in human saliva and gastric juice does not generally exceed 50 ppm. Therefore, the most probable source of mutagens--nitrosation of MTCAs and tyramine--is likely to be very restricted in vivo and soy sauce is unlikely to be significantly mutagenic.

Animals↗
PubMed1981

Approaches to a markedly increased sensitivity of the radioimmunoassay for thyrotropin-releasing hormone by derivatization.

Antisera to thyrotropin-releasing hormone (pGlu-His-Pro-NH2, TRH) have previously been produced in rabbits by immunization with a conjugate having TRH linked to a carrier protein by means of dinitrophenylene (Dnp) moiety. Studies on the specificity of the antisera obtained suggested that the sensitivity of the radioimmunoassay for TRH may be increased substantially by prior conversion of the hormone in to dinitrophenylene derivatives. To test this possibility, several TRH-Dno derivatives were prepared by reaction of TRH with equimolar amounts of 1,5-difluoro-2,4-dinitrobenzene yielding Nim-(5-fluoro-2,4-dinitrophenyl)TRH. This intermediate was reacted with ammonia, histamine, tyramine or N alpha-acetyl-lysine methyl ester (N alpha Ac-Lys-OMe) to yield the respective unsubstituted and N-substituted Nim-(5-amino-2,4-dinitrophenyl)TRH derivatives: TRH-Dnp-NH2, TRH-Dnp-histamine, TRH-Dnp-tyramine and TRH-Dnp-N alpha Ac-Lys-OMe. Nim-(2,4-Dinitrophenyl)TRH was prepared similarly by reaction of TRH with 1-fluoro-2,4-dinitrobenzene. The products were isolated by means of high-performance liquid chromatography (HPLC) and were found to be pure by HPLC and thin-layer chromatography using several solvent systems. TRH-Dnp-histamine and TRH-Dnp-tyramine were labelled with 125I using the chloramine-T method. The labelled products were purified to homogeneity by ion-exchange chromatography on SP-Sephadex and adsorption chromatography on Sephadex LH-20, respectively, and were found by HPLC to be pure.

Animals↗
PubMed1982

Effects of an extract of Ginkgo biloba on rabbit isolated aorta.

1. Extract of Ginkgo biloba (Gb) provoked a dose-dependent contraction of spirally-cut rabbit aortic strips (EC50 congruent to 1.0 mg/ml) by an action that was antagonized by phentolamine (10(-7) M). 2. Inhibitors of catecholamine re-uptake, cocaine (10(-5) M) and desipramine (10(-7) M) potentiated the contractile effect of norepinephrine (NE), but inhibited the contractile effects of Gb and tyramine. 3. A comparison of the actions of Gb, NE and tyramine using aortic strips prepared from control and reserpine-treated rabbits revealed that reserpine treatment increased the response to NE but decreased the response to Gb and tyramine. 4. The contractile action of Gb on rabbit isolated aorta involves, at least in part, a release of catecholamines from endogenous tissue stores.

Animals↗
PubMed1982

Neuropharmacology of adrenergic neurons in teleost fish.

Although this brief review is based on relatively few types of experiments in few species of teleosts, it is possible to summarize some points of interest regarding the similarities and differences in the mechanisms of adrenergic neurotransmission in fish compared to the higher vertebrates. 1. There is a substantial mixing of cranial autonomic ("parasympathetic") and spinal autonomic ("sympathetic") pathways in the cranial nerves. This close relationship between the two systems and the differences in the nature of the neurons of cranial origin (cholinergic, and non-adrenergic, non-cholinergic) and spinal origin (adrenergic, cholinergic and mixed "polynergic") gives a basis in fish also for a complex pattern of innervation of the various organs. 2. Adrenaline is the major transmitter substance in the adrenergic neurons of most teleosts studied, but there are exceptions within the same species. For instance, in the swimbladder mucosa of the cod, noradrenaline dominates, while adrenaline is the major catecholamine in most other organs innervated by adrenergic neurons. The reasons for the regional differences are not known and further studies of the rate of catecholamine turn-over in the adrenergic neurons of fish are clearly indicated. 3. Adrenoceptors of both the alpha- and the beta-type show great similarities with those of mammals. Some differences in the potencies of certain compounds (e.g., clonidine and methoxamine) exist and receptor binding studies should add valuable information about the adrenoceptors of teleosts. The existence of a subtype of beta-adrenoceptor (beta 2) has been proposed and further work is needed to confirm or deny the applicability of the beta 1/beta 2 adrenoceptor terminology in fish. 4. There appears to be some differences in the mode of action of the so called "indirectly acting amines", such as tyramine, between teleosts and mammals. While the uptake of tyramine into the nerve terminals in mammals appears to take place via the cocaine-sensitive neuronal uptake system which is also responsible for catecholamine uptake (uptake 1), tyramine uptake in cod neurons appears to be via a separate pathway. 5. Presynaptic supersensitivity of the type seen in mammals has also been demonstrated in teleost adrenergic neurons. Both denervation (chemical or surgical) and blockade of the neuronal uptake mechanism by cocaine or desipramine produce this type of supersensitivity, while post-synaptic supersensitivity has so far not been described in teleosts. The effects of removal of the uptake system shows that the uptake process may be as important in teleosts as in mammals in the removal of adrenergic transmitter from the synaptic cleft. 6. In the total picture of adrenergic functions in fish, the circulating catecholamines take a special role...

Adrenergic Fibers↗
PubMed1984

Facilitatory effect of adrenocorticotropic hormone and related peptides on Ca2+-dependent noradrenaline release from sympathetic nerves.

Strips of rabbit pulmonary artery and aorta were incubated with [3H]noradrenaline and subsequently superfused. Tritium overflow from strips superfused with physiological salt solution was stimulated either electrically (usually at a frequency of 2 Hz) or by tyramine 1 mumol/l and overflow from strips superfused with Ca2+-free solution containing K+ 54.7 mmol/l was stimulated by introduction of Ca2+ 1.6 mmol/l. In most of the experiments (stimulation by electrical impulses or CaCl2) neuronal and extraneuronal uptake and beta-adrenoceptors were blocked by cocaine, corticosterone and propranolol, respectively. The electrically evoked overflow of 3H-labelled substances from pulmonary artery and aorta was increased by adrenocorticotropic hormone. In the pulmonary artery, the adrenocorticotropic hormone--induced increase in impulse--evoked overflow (and contraction) was the more pronounced, the lower the frequency of stimulation (6, 2 and 0.66 Hz: 360 impulses). The electrically evoked overflow of 3H-labelled substances was also increased by alpha-melanocyte-stimulating hormone and porcine adrenocorticotropic hormone, but was not affected by adrenocorticotropic hormone. Adrenocorticotropic hormone also facilitated the Ca2+-evoked overflow of 3H-labelled substances promoted by high K+, but it did not affect the Ca2+-independent tyramine-evoked overflow. Adrenocorticotropic hormone did not alter the percentages of [3H]noradrenaline and 3H-labelled metabolites contained in electrically or tyramine-evoked overflow of 3H-labelled substances. In conclusion, adrenocorticotropic hormone and fragments of adrenocorticotropic hormone cause an increase in stimulation-evoked, Ca2+-dependent noradrenaline release from postganglionic sympathetic nerve fibres, probably by activating presynaptic receptors for adrenocorticotropic hormone.

Adrenocorticotropic Hormone↗
PubMed1984

In vitro occurrence of m-octopamine in the cultured cephalic ganglion of Locusta migratoria L. after L-dopa administration.

Cephalic ganglia of the locust Locusta migratoria L. were cultured in the presence of L-DOPA and inhibitors of dopa decarboxylase or dopamine beta hydroxylase. The addition of L-DOPA to the culture medium resulted in a marked increase of m-octopamine, following higher levels of dopamine. L-DOPA produced an increase of m-tyramine. RO 44602 considerably reduced the levels of p and m-octopamines, m-tyramine, dopamine and noradrenaline while fusaric acid reduced only those of p and m-octopamines, m-tyramine and noradrenaline. Though not normally found in the locust nervous system, m-octopamine appears to be closely related to catecholamines and to be produced via their biosynthesizing enzymes through a hypothetical dehydroxylation step.

Animals↗
PubMed2005

Determination of biogenic amines in chocolate by ion chromatographic separation and pulsed integrated amperometric detection with implemented wave-form at Au disposable electrode.

A rapid and selective cation exchange chromatographic method coupled to integrated pulsed amperometric detection (PAD) has been developed to quantify biogenic amines in chocolate. The method is based on gradient elution of aqueous methanesulfonic acid with post column addition of strong base to obtain suitable conditions for amperometric detection. A potential waveform able to keep long time performance of the Au disposable electrode was set up. Total analysis time is less than 20min. Concentration levels of dopamine, serotonin, tyramine, histamine and 2-phenylethylamine were measured, after extraction with perchloric acid from 2g samples previously defatted twice with petroleum ether. The method was used to determine the analytes in chocolate real matrices and their quantification was made with standard addition method. Only dopamine, histamine and serotonin were found in the analysed real samples. Repeatabilities of their signals, computed on their amounts in the real samples, were 5% for all of them. Repeatabilities of tyramine and phenethylamine were relative to standard additions to real samples (close to 1mg/l in the extract) and were 7 and 3%, respectively. Detection limits were computed with the 3s of the baseline noise combined with the calibration plot regression parameters. They were satisfactorily low for all amines: 3mg/kg for dopamine, 2mg/kg for tyramine, 1mg/kg for histamine, 2mg/kg for serotonin, 3mg/kg for 2-phenylethylamine.

Biogenic Amines↗
PubMed2005

Diuretic factors and second messengers stimulate secretion of the organic cation TEA by the Malpighian tubules of Drosophila melanogaster.

This study showed that four factors which stimulate transepithelial fluid secretion and inorganic ion transport across the main segment of the Malpighian tubules of Drosophila melanogaster also stimulate transepithelial secretion of the prototypical organic cation tetraethylammonium (TEA). TEA fluxes across the Malpighian tubules and gut were measured using a TEA-selective self-referencing (TEA-SeR) microelectrode. TEA flux across isolated Malpighian tubules was also measured using a TEA-selective microelectrode positioned in droplets of fluid secreted by tubules set up in a modified Ramsay assay. TEA flux was stimulated by the intracellular second messengers cAMP and cGMP, which increase the lumen-positive transepithelial potential (TEP), and also by tyramine and leucokinin-I (LK-I), which decrease TEP. The largest increase was measured in response to 1 micromol l-1 LK-I which increased transepithelial TEA flux by 72%. TEA flux in the lower tubule was stimulated slightly (13%) by 1 micromol l-1 tyramine but not by any of the other factors. TEA flux across the midgut was unaffected by cAMP, cGMP or tyramine. This is the first study to demonstrate the effects of insect diuretic factors and second messengers on excretion of organic cations.

Animals↗
PubMed2006

Short- and long-term insulin-like effects of monoamine oxidases and semicarbazide-sensitive amine oxidase substrates in cultured adipocytes.

Semicarbazide-sensitive amine oxidase (SSAO) is known to increase during in vitro adipogenesis and to be one of the most highly expressed membrane proteins of white adipocytes. Although less well documented, mitochondrial monoamine oxidases (MAOs) are also present in adipocytes and share with SSAO the capacity to generate hydrogen peroxide. This work therefore aimed to compare several biologic effects of MAO and SSAO substrates in 3T3-F442A adipocytes. In differentiated cells, tyramine oxidation was predominantly MAO dependent, whereas benzylamine oxidation was SSAO dependent. Both amines partially mimicked insulin actions, including stimulation of Akt phosphorylation and glucose uptake. In addition, tyramine and benzylamine impaired tumor necrosis factor alpha-dependent nitric oxide formation in a pargyline- and semicarbazide-sensitive manner, respectively. Various biogenic amines were tested in competition for tyramine or benzylamine oxidation and classified as MAO-preferring (methoxytyramine, tryptamine) or SSAO-preferring substrates (methylamine, octopamine). Short-term incubation with 1 mmol/L of all amines except histamine stimulated glucose uptake up to 20% to 50% of maximal insulin activation. One-week treatment with either MAO or SSAO substrates alone allowed postconfluent cells to differentiate into adipocytes, reproducing 60% of insulin-promoted lipid accumulation. All amines also exerted a slight improvement in the adipogenic action of insulin. Therefore, like SSAO, substrate activation of MAO can interact with adipocyte metabolism by mimicking diverse effects of insulin in addition to preventing tumor necrosis factor alpha-dependent responses.

3T3 Cells↗
PubMed1999

Effect of noradrenergic inputs on the cardiovascular depressor responses to stimulation of central nucleus of the amygdala.

Experiments were done in chloralose anesthetized, paralyzed and artificially ventilated male Wistar rats to investigate the effects of microinjections of either norepinephrine (NE) or tyramine into the central nucleus of the amygdala (ACe) on the arterial pressure (AP) and heart rate (HR) responses elicited by glutamate (Glu) stimulation of the ACe. Microinjections of Glu into the ACe elicited decreases in mean AP (-23+/-3 mmHg) and HR (-11+/-3 bpm). Microinjections of NE or tyramine into these sites did not elicit cardiovascular responses. However, Glu into the ACe in the presence of NE or tyramine elicited depressor or bradycardic response that were significantly smaller (70-100%) in magnitude than to Glu alone. These data suggest that noradrenergic mechanisms in the ACe alter the excitability of ACe neurons involved in mediating changes in systemic AP and HR.

Amygdala↗
PubMed2000

Hydrogen peroxide generation by monoamine oxidases in rat white adipocytes: role on cAMP production.

In rat, white adipocytes monoamine oxidases (EC 1.4.3.4.) generate hydrogen peroxide (H(2)O(2)). Recent studies suggested that, in addition to its toxic features, H(2)O(2) may behave as a cell second messenger. In the present study, using fluorimetric and chemiluminescence (CL) assays, we showed that tyramine degradation by monoamine oxidases in intact adipocytes resulted in the concentration-dependent generation of H(2)O(2). In addition, we found that, in the presence of low tyramine concentrations, forskolin-dependent cAMP production was significantly increased as compared to that of the control and this increase was prevented by the monoamine oxidase inhibitor pargyline or by the H(2)O(2) trapping system homovanillic acid-peroxidase. Finally, we demonstrated that tyramine degradation by monoamine oxidases increased the ability of isoproterenol to induce cell lipolysis. Taken together, these data suggest that H(2)O(2) produced during substrate degradation by monoamine oxidases may participate in the regulation of adipocyte metabolism.

Adipocytes↗