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PubMed1998

Oculosympathetic alterations in migraine patients.

Oculosympathetic function was studied in 20 headache-free migraine patients and in 20 controls. Pupillary investigation was performed under basal conditions, and after instillation of tyramine (2%) and phenylephrine (1%) eyedrops. Each test was performed twice shortly after a spontaneous attack and then repeated after 7 and 15 days. In the patients, the normal mydriatic response induced by tyramine was significantly (p<0.001) reduced and phenylephrine instillation caused a significant (p<0.01) pupillary dilatation in both the assessments performed shortly after the attack. These abnormal responses were bilateral in all patients and slightly anisocoric in some. They were significantly (p<0.001) more pronounced in the patients who had pain and pronounced vascular features. The reduced oculosympathetic response to tyramine, as well as the hypersensitivity to phenylephrine, was less evident 7 days after the attack and absent after 15 days. A transient and bilateral post-ganglionic oculosympathetic hypofunction, with adrenoceptor hypersensitivity, was found to be temporally related to the migraine attack, regardless of the side or predominant side of pain.

Adult↗
PubMed1995

Structural requirements for cocaine-sensitive and -insensitive uptake of phenethylamines into the adrenal chromaffin cell.

The adrenal medullary chromaffin cell is a commonly used model for the adrenergic neuron. Although much work has been done to study the transport system in the adrenal chromaffin vesicles, relatively little is known about cellular transport, especially with regard to structural features of phenethylamines required for intracellular accumulation. We have now investigated the structural requirements of phenethylamine-related compounds for their accumulation into cultured adrenal chromaffin cells. We find that two types of cellular uptake, previously described only for dopamine, norepinephrine, and epinephrine, are also present for [3H]tyramine. Although two types of accumulation occur, tyramine accumulation occurs mainly via a cocaine-insensitive process, whereas dopamine accumulation occurs predominantly via a cocaine-sensitive process. The accumulation of [14C]-phenethylamine and p-methoxyphenethylamine is not affected by cocaine, suggesting that a ring hydroxyl substituent is necessary for cocaine-sensitive accumulation. The compounds p-hydroxyphenylpropylamine and p-hydroxyphenyl-2-aminoethyl sulfide accumulate in the cell only via a cocaine-insensitive process, indicating that lengthening of the aminoalkyl side chain prevents cocaine-sensitive accumulation. We have performed conformational analyses of this series of compounds to determine whether the conformation of these compounds can be related to the kinetic data. For dopamine, tyramine, phenethylamine, and p-methoxyphenethylamine, two groups of energy-minimized conformers were found. We find that there is an approximately linear relationship between the Km values for these phenethylamines and the differences in minimized energies between the low- and highest energy conformer groups of each compound. A similar correlation was found for p-hydroxyphenyl-2-aminoethyl sulfide. These results are consistent with the hypothesis that these compounds undergo a conformational change from the low-energy conformer to the highest energy conformer before their cocaine-insensitive accumulation.

Adrenal Glands↗
PubMed1998

Relationships between the catechol substrate binding site and amphetamine, cocaine, and mazindol binding sites in a kinetic model of the striatal transporter of dopamine in vitro.

Experiments were conducted to determine how (-)-cocaine and S(+)-amphetamine binding sites relate to each other and to the catechol substrate site on the striatal dopamine transporter (sDAT). In controls, m-tyramine and S(+)-amphetamine caused release of dopamine from intracellular stores at concentrations > or = 12-fold those observed to inhibit inwardly directed sDAT activity for dopamine. In preparations from animals pretreated with reserpine, m-tyramine and S(+)-amphetamine caused release of preloaded dopamine at concentrations similar to those that inhibit inwardly directed sDAT activity. S(+)-Amphetamine and m-tyramine inhibited sDAT activity for dopamine by competing for a common binding site with dopamine and each other, suggesting that phenethylamines are substrate analogues at the plasmalemmal sDAT. (-)-Cocaine inhibited sDAT at a site separate from that for substrate analogues. This site is mutually interactive with the substrate site (K(int) = 583 nM). Mazindol competitively inhibited sDAT at the substrate analogue binding site. The results with (-)-cocaine suggest that the (-)-cocaine binding site on sDAT is distinct from that of hydroxyphenethylamine substrates, reinforcing the notion that an antagonist for (-)-cocaine binding may be developed to block (-)-cocaine binding with minimal effects on dopamine transporter activity. However, a strategy of how to antagonize drugs of abuse acting as substrate analogues is still elusive.

Amphetamine↗
PubMed1998

Voltammetric studies on mechanisms of dopamine efflux in the presence of substrates and cocaine from cells expressing human norepinephrine transporter.

The effects of substrates m-tyramine and beta-phenethylamine, as well as cocaine, on the DA efflux from a cell line stably expressing the human norepinephrine transporter (hNET) were investigated by using rotating disk electrode voltammetry. Both the substrates and cocaine induced apparent DA efflux in a concentration-dependent manner. Their EC50 values for inducing DA efflux were similar to their IC50 values for inhibiting DA uptake. The substrate-induced DA efflux was inhibited by various NET blockers, enhanced by raising the internal [Na+] with Na+,K+-ATPase inhibition, but was insensitive to membrane potential-altering agents valinomycin, veratridine, and high [K+]. The initial rate of m-tyramine-induced DA efflux was related to preloaded [DA] in a manner defined by a Michaelis-Menten expression. In contrast, DA efflux in the presence of cocaine displayed a much slower efflux rate, lower efficacy, was not stimulated by elevated internal [Na+], and was nonsaturable with preloaded [DA]. Single exponential kinetic analysis of the entire time course of the DA efflux showed that the apparent first-order rate constant for m-tyramine-induced DA efflux declined with increased preloaded [DA], whereas that for the DA efflux in the presence of cocaine was unchanged with varying preloaded [DA]. These results suggest that the substrates stimulate the NET-dependent DA efflux by increasing the accessibility of the NET to internal DA, whereas cocaine "uncovers" NET-independent DA efflux by reducing the accessibility of diffused/leaked external DA to the NET.

Adrenergic Uptake Inhibitors↗
PubMed1997

The enhanced ciliospinal reflex in asymptomatic patients with cluster headache is due to preganglionic sympathetic mechanisms.

An amplified ciliospinal reflex response has been documented in patients with cluster headache, lacking a Horner-like syndrome. The mechanism is unknown. Tentatively, it may be due to an increased release of monoamines from post-ganglionic sympathetic nerve endings or an increased density of postsynaptic adrenergic receptors in the dilatator muscle of the iris. The instillation of a 1% phenylephrine solution into the conjunctival sac induces mydriasis by stimulating postsynaptic adrenergic receptors in the dilatator muscle of the iris, while the instillation of a 2% tyramine solution causes mydriasis by releasing noradrenaline from the presynaptic sympathetic nerve terminals in the iris. According to these premises, a positive correlation should be expected between the ciliospinal reflex response and the pupillary response to tyramine, if the enhanced ciliospinal reflex response was due to an increased presynaptic release of monoamines. No such correlation was found. Nor was there any positive correlation between the ciliospinal reflex response and the pupillary response to phenylephrine, contradicting an increased density of postsynaptic monoaminergic receptors in the dilatator muscle of the iris as the explanation. However, there was a significant positive correlation between the pupillary responses to phenylephrine and tyramine, ruling out any functionally caused "denervation" hypersensitivity in the dilatator muscle of the iris. It is concluded that the amplified ciliospinal reflex response in cluster headache patients (lacking a Horner-like syndrome) reflects compensatory pathophysiological mechanisms proximal to the third-order sympathetic neuron.

Adult↗
PubMed2000

Transport-dependent accessibility of a cytoplasmic loop cysteine in the human dopamine transporter.

The effect of covalent sulfhydryl modification on dopamine uptake by the human dopamine transporter was determined by rotating disc electrode voltammetry. A transporter construct, X5C, with five mutated cysteines (C90A, C135A, C306A, C319F, and C342A) and the constructs into which the wild-type cysteines were substituted back into X5C, one at a time, all showed nearly normal binding affinity for [(3)H]CFT and for cocaine, but they displayed significant reductions in K(m) and V(max) for DA uptake. Reaction of Cys-90 or Cys-306 with impermeant methanethiosulfonate derivatives enhanced dopamine uptake to a similar extent as the previously observed enhancement of [(3)H]CFT binding caused by the same reaction, suggesting that cocaine may bind preferentially to a conformation in the transport cycle. m-Tyramine increased the rate of reaction of (2-aminoethyl)methanethiosulfonate (MTSEA) with X-A342C, the construct with a cytoplasmic loop residue Cys-342 restored. This m-tyramine-induced increase in reactivity appeared to require the inward transport rather than the outward transport or external binding of m-tyramine, and it was prevented by cocaine. Thus, inward translocation of substrates may involve structural rearrangement of hDAT, which likely exposes Cys-342 to reaction with MTSEA, and Cys-342 may be located on a part of the transporter associated with cytoplasmic gating.

Biological Transport↗
PubMed2005

Metabolic flux analysis of the phenylpropanoid pathway in elicitor-treated potato tuber tissue.

The effects of beta-1,3-oligosaccharide elicitor on the metabolism of phenylpropanoids in potato tuber were analyzed quantitatively, by monitoring the time-dependent changes in the levels of seven compounds. The elicitor treatment caused an increase in the pool size of octopamine and tyramine amides (N-p-coumaroyloctopamine, N-feruloyloctopamine, N-p-coumaroyltyramine and N-feruloyltyramine), as well as a decrease in that of chlorogenic acid and putrescine amides (caffeoylputrescine and feruloylputrescine). An analysis of metabolic flux using stable isotope labeling and liquid chromatography-spectrometry (LC-MS) detection clearly demonstrated that the changes in the pool size of these compounds were correlated with the changes in their flux for biosynthesis (Jin) upon elicitor treatment. The increase in Jin in the cases of octopamine and tyramine amides was accompanied by an increase in flux for the transformation (Jout), indicating a rapid turnover of these compounds in the elicitor-treated tuber tissue. The result of the flux analysis indicated that the actual activation of the biosynthesis of octopamine and tyramine amides after the elicitor treatment was greater than that estimated from the changes in their levels in the potato tissue. These findings suggest that these amide compounds and their metabolic derivatives play an important role in the defense-related metabolism of phenylpropanoids in potato.

Amides↗
PubMed1975

Venomotor changes caused by halothane acting on the sympathetic nerves.

Experiments were performed to determine whether depression of venomotor responses with halothane results from interference with sympathetic activation or from an effect on venous smooth muscle cells. Changes in isometric tension of isolated canine saphenous-vein strips were recorded. Adrenergic activation was achieved by transmural electrical stimulation, by addition of tyramine, and by addition of morepinephrine. Halothane (0.5 to 3 per cent) did not significantly alter basal tension. It lessened the reaction of the veins to electrical stimulation but not their response to norepinephrine; it increased the response to tyramine. Since the responses to norepinephrine and tyramine were not decreased, halothane appears to act on the nerve terminal to prevent release of neurotransmitter associated with nerve-terminal depolarization. Thus, halothane causes inhibition of electrically induced venoconstriction in cutaneous veins, probably by interfering with the release of norepinephrine from nerve terminals rather than by an inhibitory effect on the smooth muscle cells.

Anesthesia, Inhalation↗
PubMed1997

The effects of RS-8359 on cardiovascular function in healthy subjects and depressed patients.

The potential liability of RS-8359 for the 'cheese' effect that is characteristic of the classical monoamine oxidase inhibitors has been compared with placebo and moclobemide in the tyramine test. Both RS-8359 and moclobemide reduce the dose of tyramine required to raise systolic blood pressure by 30 mmHg by about half, but the risk of the tyramine interaction is not clinically significant at this level. This low risk is confirmed by the very low incidence of cardiovascular adverse events reported in early clinical studies and by the lack of any material changes in blood pressure. These results indicate that no dietary restrictions will be required when RS-8359 is used clinically.

Adult↗
PubMed1988

Augmenting effect of a nonmutagenic fraction in soy sauce on mutagenicity of 3-diazotyramine produced in the nitrite-treated sauce.

When 25 kinds of Japanese soy sauce at a concentration of 5% were incubated with 50mM sodium nitrite (pH 2) at 37 degrees for 1 hr, the reaction mixtures induced 34-834 (average 368 +/- 228) revertants per microliter of soy sauce equivalent in Salmonella typhimurium strain TA100 in the absence of S9 mix. The mutagen(s) formed was very unstable under natural daylight and a fluorescent lamp but quite stable under a yellow lamp as well as in the dark. In addition to the known precursors, i.e., tyramine and 1-methyl-1,2,3,4-tetrahydro-beta-carboline-3-carboxylic acid, 1-methyl-1,2,3,4-tetrahydro-beta-carboline, which caused weak mutagenesis, was found in the soy sauce. However, the sum of the activities of the three mutagen-precursors after nitrite treatment accounted for only a part of the mutagenicity of nitrite-treated soy sauce. There was in the soy sauce a factor which increased ninefold the mutagenicity of nitrite-treated tyramine, 3-diazotyramine. Therefore, tyramine was considered the principal precursor of the mutagen produced in the nitrite-treated soy sauce. These three precursors together with the mutagenicity augmentation accounted for all the mutagenicity of nitrite-treated sauce. The mutagenicity-augmenting factor in the soy sauce was nonmutagenic before and after nitrite treatment and was stable to heat and light irradiation.

Carbolines↗
PubMed2006

Safety properties and molecular strain typing of lactic acid bacteria from slightly fermented sausages.

AIM: To evaluate the biodiversity of lactobacilli from slightly fermented sausages (chorizo, fuet and salchichon) by molecular typing, while considering their safety aspects. METHODS AND RESULTS: Species-specific PCR, plasmid profiling and randomly amplified polymorphic DNA (RAPD)-PCR were used to characterize 250 lactic acid bacteria (LAB) isolated from 21 low acid Spanish fermented sausages. Lactobacillus sakei was the predominant species (74%) followed by Lactobacillus curvatus (21.2%) and Leuconostoc mesenteroides (4.8%). By plasmid profiling and RAPD-PCR 144 different strains could be differentiated, 112 belonging to Lact. sakei, 23 to Lact. curvatus and 9 to Leuc. mesenteroides. Ion-pair high performance liquid chromatography was used to detect biogenic amine production. Tyramine and phenylethylamine were produced by 14.4 and 12.4% of the isolates, respectively, all belonging to the species Lact. curvatus. The production of tyramine was stronger than that of phenylethylamine. Partial sequencing of the tyrosine decarboxylase gene from Lact. curvatus was achieved. A specific PCR assay to detect the Lact. curvatus tyramine-producers was designed. The disc diffusion test was used to detect antibiotic resistance among the isolates. Most isolates displayed resistance to vancomycin and gentamicin. Only four strains were resistant to most of the antibiotics tested. None of the isolates were resistant to erythromycin. CONCLUSIONS: Lactobacillus sakei would be the species of choice for further use as starter culture in fermented sausage production. Strain typing and characterization of biogenic amine production together with antibiotic susceptibility testing for the selection of starter cultures could help to increase the quality and safety of the products. SIGNIFICANCE AND IMPACT OF THE STUDY: Species-specific PCR, RAPD and plasmid profiling proved to be efficient at typing LAB at species and strain level. Information on biogenic amine production and transferable antibiotic resistance is important in order to avoid selection of strains with undesirable properties as starter cultures.

Animals↗
PubMedDate not supplied

Some cardiovascular effects of monoamine oxidase inhibitors in unanaesthetized rats.

The effects of four monoamine oxidase (MAO) inhibitors on the blood pressure of conscious normotensive and DOC-salt hypertensive rats were measured. Harmaline (20 mg/kg p.o.), pargyline (100 mg/kg p.o.) and tranylcypromine (10 mg/kg p.o.) all lowered blood pressure significantly in both normotensive and hypertensive rats whereas methylaplysinopsin (10 mg/kg p.o.) had no effect on blood pressure. The effects of these MAO inhibitors on blood pressure responses to serotonin, tyramine and beta-phenylethylamine were determined in conscious normotensive rats. Pargyline and tranylcypromine shifted the dose-response curves for tyramine and beta-phenylethylamine, but not serotonin, to the left, indicating inhibition of type B MAO. Harmaline and methylaplysinopsin shifted the dose-response curves for tyramine and serotonin but not beta-phenylethylamine, to the left, indicating inhibition of type A MAO. Since the four antagonists tested inhibited at least one form of MAO, and yet not all of these MAO inhibitors lowered blood pressure, we suggest that our results are consistent with the view that the hypotensive action of MAO inhibitors is not necessarily related to inhibition of MAO.

Anesthesia↗
PubMed1982

Monoamine oxidase activity of mitochondria prepared from rat liver and rat heart.

The effect of agents that change the respiratory state of the mitochondrion on tyramine oxidation was investigated. Neither uncoupler nor ADP and P1 in the presence of substrate produced any change in the rate of tyramine oxidation, as judged by direct measurement of tyramine oxidation or by H2O2 production. We conclude that previously reported depression of monoamine oxidase activity by stimulated respiration was due to oxygen depletion.

Animals↗
PubMed1985

Sulfate conjugation of monoamines in human brain: purification and some properties of an arylamine sulfotransferase from cerebral cortex.

An arylamine sulfotransferase (PST-M) from human brain cortex that is involved in the formation of O-sulfate esters of monoamines has been purified 272-fold by ammonium sulfate fractionation, gel filtration, DEAE-cellulose ion-exchange chromatography, chromatofocussing, and hydroxyapatite chromatography. A molecular weight of 62,000, pK of pH 5.8, and an optimum pH for the reaction at 7.8-8.0 with respect to tyramines have been determined. This enzyme possesses an extremely high affinity for dopamine and m-tyramine based on the low Km values and is moderately active toward noradrenaline and p-tyramine. Serotonin is a poor substrate. In contrast, another sulfotransferase, PST-P, which has been separated from PST-M and partially purified, exhibited a very high affinity for phenol and nitrophenols but was inactive toward the amine sulfate acceptors. In the human brain the specific activity toward dopamine as well as the ratio of activity toward dopamine/phenol was considerably higher than those for rat, hog, and bovine brains.

Aged↗
PubMed1986

A and B forms of monoamine oxidase within the monoaminergic neurons of the rat brain.

The inhibition of the A and B forms of monoamine oxidase (MAO) inside and outside serotonergic, noradrenergic, and dopaminergic synaptosomes in homogenates of rat hypothalamus or striatum by clorgyline, a selective and irreversible MAO-A inhibitor, and selegiline, a selective and irreversible MAO-B inhibitor, was examined. Intrasynaptosomal deamination at low concentrations of the substrates [14C]5-hydroxytryptamine ([14C]5-HT; 0.1 microM), [14C]noradrenaline (0.25 microM), [14C]3,4-dihydroxyphenylethylamine ([14C]dopamine; 0.25 microM), and [14C]tyramine (0.25 microM) was hindered by selective uptake inhibitors (citalopram, maprotiline, and amfonelic acid) in the incubation media. Thus, the difference between the deamination of 14C-amine in the absence and presence of the appropriate selective uptake inhibitor provided a measure of deamination in the specific aminergic synaptosomes. This was verified by determining the loss of MAO activity within noradrenergic and serotonergic systems after degeneration of the nerve terminals by the neurotoxins N-chloroethyl-N-ethyl-2-bromobenzylamine and p-chloroamphetamine. Results with the two inhibitors revealed that the A and B forms were responsible for 80 and 20%, respectively, of the deamination of [14C]5-HT within serotonergic synaptosomes from the hypothalamus. The deamination of [14C]noradrenaline within the noradrenergic synaptosomes from the hypothalamus and that of [14C]dopamine and [14C]tyramine within the striatal dopaminergic synaptosomes were due to MAO-A. About 10% of the deamination of [14C]noradrenaline, [14C]dopamine, and [14C]tyramine outside the noradrenergic or dopaminergic synaptosomes was brought about by the B form, with the remainder being deaminated by MAO-A.

Amines↗
PubMed1961

Effects of cocaine and antidepressant drugs on the nictitating membrane of the cat.

Cocaine, imipramine and pipradol potentiated the contractions to adrenaline and noradrenaline, but not to tyramine, on the nictitating membrane of the spinal cat. Pheniprazine and dexamphetamine potentiated the responses to adrenaline, noradrenaline and tyramine, whereas nialamide only potentiated the response to tyramine. Potentiation of the response to stimulation of either the preganglionic or the postganglionic sympathetic nerve trunks was observed with imipramine, pipradol, pheniprazine and dexamphetamine. Only dexamphetamine and pheniprazine caused substantial contractions of the membrane when the preganglionic nerve was cut (acutely decentralized), or when the superior cervical ganglion was removed (acutely denervated). Cocaine produced contractions of the innervated but not of the acutely decentralized membrane. The significance of the peripheral effects of these antidepressant drugs in relation to their central actions is discussed.

Animals↗
PubMed1968

Action of various sympathomimetic amines on the isolated stripped vas deferens of the guinea-pig.

1. The contractile potencies of some sympathomimetic amines and cholinergic drugs were studied in the isolated, stripped vas deferens of the guinea-pig.2. alpha-Methylnoradrenaline, adrenaline and metaraminol produced the same relative maximal responses as noradrenaline, which served as reference drug; on the other hand, octopamine, dopamine and alpha-methyldopamine were much less active. Short term pretreatment of the animals with reserpine did not affect the maximal relative responses.3. Tyramine, alpha-methyl-m-tyramine and hordenine methiodide had little effect on the untreated preparation. In the presence of just threshold concentrations of noradrenaline, the relative maximal responses to tyramine and hordenine methiodide were markedly increased.4. The relative maximal response to carbachol was the same as that to noradrenaline, while that to DMPP was smaller. In contrast to carbachol, the action of DMPP was potentiated by pretreatment of the preparation with noradrenaline.

Animals↗
PubMed1968

The interaction between angiotensin and sympathetic vasoconstriction in the isolated artery of the rabbit ear.

1. Infusions or injections of angiotensin into the isolated ear artery preparation of the rabbit produced only feeble vasoconstrictions and depressed the sensitivity of the preparation to sympathetic stimulation, tyramine and noradrenaline.2. The anti-sympathetic effect of angiotensin was not prevented or reversed by noradrenaline or cocaine.3. The vasoconstrictor response to angiotensin was usually markedly increased during sympathetic stimulation or other procedures which liberate endogenous noradrenaline (for example, infusion of tyramine), but not when the perfusion pressure was raised by increasing the flow rate or by infusing noradrenaline.4. The vasoconstrictor action of tyramine was also potentiated by sympathetic stimulation.5. The potentiation by sympathetic stimulation of the responses to angiotensin was prevented by reserpine, guanethidine and phentolamine in concentrations which abolished sympathetic vasoconstriction.6. It is suggested that angiotensin facilitates the release of endogenous noradrenaline and owes part of its vasoconstrictor activity to this property.

Angiotensin II↗