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At least 1,711 records · Page 95Linked to original sources
PubMed2002

Lignanamides and nonalkaloidal components of Hyoscyamus niger seeds.

Four lignanamides, a tyramine derivative, and 10 other nonalkaloidal components were isolated from the seeds of Hyoscyamus niger. Among them, hyoscyamide (1), 1,24-tetracosanediol diferulate (6), and 1-O-(9Z,12Z-octadecadienoyl)-3-O-nonadecanoyl glycerol (7) are new structures. The other compounds were identified as grossamide, cannabisin D, cannabisin G, N-trans-feruloyl tyramine, 1-O-octadecanoyl glycerol, 1-O-(9Z,12Z-octadecadienoyl) glycerol, 1-O-(9Z,12Z-octadecadienoyl)-2-O-(9Z,12Z-octadecadienoyl) glycerol, 1-O-(9Z,12Z-octadecadienoyl)-3-O-(9Z-octadecenoyl) glycerol, rutin, vanillic acid, beta-sitosterol, and daucosterol. Grossamide, and cannabisins D and G exhibited moderate cytotoxicity in cultured LNCaP human prostate cancer cells.

China↗
PubMed2006

Antiplasmodial metabolites isolated from the marine octocoral Muricea austera.

Bioassay-guided fractionation of the MeOH extract from the octocoral Muricea austera collected in the Pacific coast of Panama led to the isolation of eight compounds, including three tyramine derivatives (1-3), two steroidal pregnane glycosides (4, 5), and three sesquiterpenoids (6-8). Compounds 2-5 are new natural products, and their structures were determined on the basis of their spectroscopic data (HRMS, 1D and 2D NMR, and CD studies). The antiprotozoal activities of the natural compounds 1-8 as well as those of a series of synthetic glycosides (11-22) and tyramine derivatives (23-35) were evaluated in vitro against a drug-resistant Plasmodium falciparum and intracellular form of Trypanosoma cruzi.

Animals↗
PubMed2003

Modulatory inputs on sympathetic neurons in the rostral ventrolateral medulla in the rat.

1. The first part of this study looks at spontaneously active neurons located in the rostral ventrolateral medulla (RVLM) with projections to the thoracic spinal cord. Sixteen neurons were intracellularly recorded in vivo. Four out of 16 neurons were antidromically activated from the thoracic spinal cord (axonal conduction velocities varied from 1.8 m/s to 9.5 m/s). 2. The simultaneous averages of the neuronal membrane potential and arterial blood pressure triggered by the pulsatile arterial wave or the EKG-R wave demonstrated changes in membrane potential (hyperpolarization or depolarization) locked to the cardiac cycle in four neurons in this group. These neurons (three of them bulbospinal) were further tested for barosensitivity by characterizing the responses to electrical stimulation of the aortic depressor nerve. Four neurons responded with inhibitory hyperpolarizing responses characterized as inhibitory postsynaptic potentials (IPSP) to aortic nerve stimulation (onset latency: 32.3 +/- 5.0 ms; mean +/- SEM). 3. In two neurons in the RVLM, one of them characterized as barosensitive, electrical stimulation of the opposite RVLM (0.5 Hz, 1.0 ms pulse duration, 25-100 microA) elicited excitatory postsynaptic potentials (EPSPs) with latencies of 9.07 and 10.5 ms. At resting membrane potential, the onset latency of the evoked EPSPs did not change with increasing stimulus intensities. Some of the recorded neurons were intracellularly labelled with biocytin for visualization. They were found in the RVLM. 4. These experiments in vivo would support the idea of a functional commissural pathway between the RVLM of both sides. 5. Anatomical data have shown that some of those commissural bundle fibers originate in the C1 adrenergic neuronal group in the RVLM. In the second part of this study, we used an intracellular recording technique in vitro to investigate the effects of the indirect adrenergic agonist tyramine on neurons in the RVLM with electrophysiological properties similar to premotor sympathetic neurons in vivo. 6. Tyramine (0.5-1 mM) produced a pronounced inhibitory effect with hyperpolarization and increase in membrane input resistance on two neurons characterized as regularly firing (R), and on one neuron characterized as irregularly firing (1). This effect was preceded by a transient depolarization with increases in firing rate. 7. These results would indicate that neurons in the RVLM recorded in vitro and with properties similar to premotor sympathetic neurons can be modulated by catecholamines released from terminals probably making synaptic contacts.

Action Potentials↗
PubMed1986

Effect of diclofensine, a novel antidepressant, on peripheral adrenergic function.

Diclofensine is a novel antidepressant with equipotent inhibitive effects on the neuronal uptake of norepinephrine (NE), serotonin, and dopamine. It is devoid of monoamine-releasing or monoaminoxidase-inhibiting properties. The action of diclofensine on peripheral neuronal adrenergic function was studied through tests of the blood pressure response to NE, tyramine, and phenylephrine (PE). The blood pressure response to NE was enhanced and that to tyramine was decreased by diclofensine, as a result of its inhibitive action on peripheral neuronal amine uptake. PE sensitivity was also enhanced by diclofensine as well as after a single dose of desmethylimipramine (DMI). In contrast to the common opinion that PE does not interact with the neuronal uptake mechanism, the increase in PE-induced blood pressure response after diclofensine and DMI suggests that PE, a nonbiogenic amine, does indeed enter into the peripheral adrenergic neuron. This neuronal uptake may probably be unmasked only by powerful NE uptake inhibitors such as DMI or diclofensine.

Administration, Oral↗
PubMed1992

Long-term ergotamine abuse: effect on adrenergically induced mydriasis.

The mydriatic action of sympathomimetic eyedrops after a therapeutic dose of ergotamine was measured in migraine patients with and without histories of long-term ergotamine abuse. Mydriasis induced by the postsynaptic alpha 1-agonist phenylephrine was similar in both groups of patients tested, whereas pupillary dilation caused by the release of noradrenaline tyramine was markedly greater in patients with histories of ergotamine abuse. The enhanced response to tyramine disappeared after drug withdrawal. These findings indicate that continuous ergotamine medication causes a reversible alterations in iris sympathetic transmission. This manifestation may reflect a central inhibition of pupillary sympathetic activity.

Adult↗
PubMed1981

Vascular responses to REN-293 (2-amino-3[3, 5-dihydroxyphenyl]-1-propanol hydrochloride)--a new sympathomimetic agent.

In this study the effects of REN-293 have been examined on the rat tail artery "in situ'. It was found that the drug was totally dependent on the sympathetic nerves for its vasoconstrictor action. This action was blocked by phentolamine and attenuated by pre-treatment of the vessel with tyramine. When a comparative study of the vasoconstrictor effects of several sympathomimetics was performed, it was found that REN-293 was more potent than tyramine and ephedrine, but less so than etilefrine. It would appear that REN-293 is of interest as a pharmacological tool for examining sympathetic nerve function, but its usefulness in the therapy of orthostatic hypotension is likely to be limited, due to the very indirect nature of its sympathomimetic action.

Animals↗
PubMed2004

Alteration of amine oxidase activity in the adipose tissue of obese subjects.

OBJECTIVE: To explore the activity of monoamine oxidases (MAOs) and semicarbazide-sensitive amine oxidases (SSAOs) in adipose tissue and blood of lean and moderately obese subjects and to study whether there is a link between these hydrogen peroxide-generating enzymes and blood markers of oxidative stress. RESEARCH METHODS AND PROCEDURES: Nine obese male subjects (BMI 32.6 +/- 0.4 kg/m(2)) and nine controls (BMI 23.4 +/- 0.5) of 24- to 40-year-old subjects were included in the study. MAO and SSAO activities were measured on microbiopsies of abdominal subcutaneous adipose tissue by quantifying (14)C-tyramine and (14)C-benzylamine oxidation. Levels of soluble SSAO, lipid peroxidation products, and antioxidant agents were measured in plasma, whereas cytoprotective enzymes were determined in blood lysates. RESULTS: The high MAO activity found in adipose tissue was diminished by one-half in obese subjects (maximum initial velocity of 1.2 vs. 2.3 nmol tyramine oxidized/mg protein/min). There was no change in SSAO activity, either under its adipose tissue-bound or plasma-soluble form. Plasma levels of lipid peroxidation products and antioxidant vitamins remained unmodified, as well as erythrocyte antioxidant enzymes, whereas circulating triglycerides, insulin, and leptin were increased. DISCUSSION: Although they already exhibited several signs of endocrino-metabolic disorders, the obese men did not exhibit the increase in blood markers of oxidative stress or the decrease in antioxidant defenses reported to occur in very obese or diabetic subjects. The reduced MAO and the unchanged SSAO activities found in obesity suggest that these hydrogen peroxide-generating enzymes expressed in adipocytes are probably not involved in the onset of the oxidative stress found in severe obesity and/or in its complications.

Abdomen↗
PubMed2001

Amine oxidase substrates mimic several of the insulin effects on adipocyte differentiation in 3T3 F442A cells.

We have previously reported that substrates of monoamine oxidase (MAO) and semicarbazide-sensitive amine oxidase (SSAO) exert short-term insulin-like effects in rat adipocytes, such as stimulation of glucose transport. In the present work, we studied whether these substrates could also mimic long-term actions of insulin. Adipose differentiation of 3T3 F442A cells, which is highly insulin-dependent, served as a model to test the effects of sustained administration of amine oxidase substrates. Daily treatment of confluent cells with 0.75 mM tyramine (a substrate of MAO and SSAO) or benzylamine (a substrate of SSAO) over 1 week caused the acquisition of typical adipocyte morphology. The stimulation of protein synthesis and triacylglycerol accumulation caused by tyramine or benzylamine reached one half of that promoted by insulin. This effect was insensitive to pargyline (an MAO inhibitor), but was inhibited by semicarbazide (an SSAO inhibitor) and by N-acetylcysteine (an antioxidant agent), suggesting the involvement of the H(2)O(2) generated during SSAO-dependent amine oxidation. Chronic administration of amine oxidase substrates also induced the emergence of adipose conversion markers, such as aP2, glycerol-3-phosphate dehydrogenase, the glucose transporter GLUT4, and SSAO itself. Moreover, cells treated with amines acquired the same insulin sensitivity regarding glucose transport as adipocytes classically differentiated with insulin. In all, most of the adipogenic effects of amines were additive to insulin. Our data reveal that amine oxidase substrates partially mimic the adipogenic effect of insulin in cultured preadipocytes. Furthermore, they suggest that SSAO not only represents a novel late marker of adipogenesis, but could also be directly involved in the triggering of terminal adipocyte differentiation.

3T3 Cells↗
PubMed1971

The kinetics of phenethylhydrazine oxidation by monoamine oxidase.

1. In the presence of the substrate benzylamine, phenethylhydrazine has been shown to be a competitive inhibitor of monoamine oxidase from rat liver and pig brain. 2. Phenethylhydrazine is also a substrate for monoamine oxidase. Reciprocal plots for hydrazine oxidation give families of intersecting lines in contrast with the parallel lines previously reported for tyramine oxidation. 3. Two possible modifications of the mechanism obeyed by tyramine oxidation are suggested, but the product inhibition results are insufficient to distinguish between these two mechanisms.

Amines↗
PubMed1975

Studies on the Arylsulphatase and phenol sulphotransferase activities of Aspergillus oryzae.

1. Crude extracts of Aspergillus oryzae grown under conditions of sulphur limitation possess high arylsulphatase activity. 2. This activity can be greatly enhanced by the inclusion of tyramine or a number of other phenols in the assay medium. 3. The arylsulphatase activity of these extracts can be resolved into three distinct fractions by chromatography on DEAE-cellulose. 4. The effect of tyramine is restricted to one of these fractions only. 5. Evidence is presented which indicates that this effect is the consequence of a phenol sulphotransferase activity, which shows no requirement for 3'-phosphoadenosine 5'-phosphate as a cofactor, and which will not transfer sulphate from 3'-phosphoadenosine 5'-sulphatophosphate to potential phenolic acceptors. 6. The three enzymes differ also in their molecular weights and substrate specificities.

Arylsulfatases↗
PubMed1977

The role of the false neurotransmitter octopamine in the hypotension of fulminant hepatic failure.

1. An investigation was carried out into the mechanism of unexplained hypotension in patients with fulminant hepatic failure. The cardiac output and peripheral resistance were compared in normotensive and hypotensive patients. In addition, the serum concentration of the false neurotransmitter octopamine and the pressor response to noradrenaline, and to the indirectly acting sympathomimetic agent tyramine, were measured in hypotensive and normotensive patients with fulminant hepatic failure and in healthy subjects. 2. The cardiac output and the peripheral resistance were decreased in the hypotensive patients, and their mean heart rate was slower than in the normotensive patients. Although the serum octopamine concentration was significantly elevated in the patients compared with the control subjects, the highest octopamine concentrations were unexpectedly found in the normotensive patients and a significant positive correlation could be demonstrated between the resting blood pressure and the serum octopamine concentration. The pressor response to tyramine and noradrenaline were similar in the hypotensive patients, the normotensive patients and control subjects. 3. These results suggest that neither increased serum concentrations of the false neurotransmitter octopamine, nor end-organ insensitivity to released noradrenaline are responsible for the hypotension. A more likely explanation is toxic depression of the vasomotor centre. The opening of peripheral arteriovenous shunts, possibly as a result of endotoxaemia, might be an additional factor.

Cardiac Output↗
PubMed1994

Plasma levels of 5-hydroxytryptamine during sympathetic stimulation and in Raynaud's phenomenon.

1. The involvement of plasma 5-hydroxytryptamine in normal subjects during sympathetic stimulation and in patients with Raynaud's phenomenon was studied. 2. Arterial and venous plasma levels of 5-hydroxytryptamine were measured in normal subjects in a warm room, during reflex sympathetic stimulation by body cooling and during intra-arterial infusions of tyramine. Normal subjects (n = 19) had significantly higher levels of 5-hydroxytryptamine in venous plasma [mean 1.42 (SEM 0.23) ng/ml] than in arterial plasma [0.67 (0.12) ng/ml; P < 0.01]. Body cooling (n = 10) or tyramine infusion (n = 8) did not increase venous levels of 5-hydroxytryptamine despite significant decreases in blood flow and increases in vascular resistance. 3. Venous plasma levels of 5-hydroxytryptamine were also determined in patients with primary Raynaud's phenomenon (n = 12) or secondary Raynaud's phenomenon due to scleroderma (n = 11). Patients with primary or secondary Raynaud's phenomenon did not have significantly higher venous plasma levels of 5-hydroxytryptamine than normal subjects, even during vasospastic attacks (n = 3). 4. It is concluded that either 5-hydroxytryptamine is not involved in sympathetic nerve vasoconstriction or in Raynaud's phenomenon, or 5-hydroxytryptamine released in the microcirculation is largely taken up or metabolized by endothelial cells or platelets.

Adult↗
PubMed1994

Alpha- and beta-cell function in obese Zucker (fa/fa) rats: a study with the isolated perfused pancreas.

1. The effects of various stimuli, including changes in glucose concentration, arginine, tyramine and noradrenaline, on insulin and glucagon secretion were investigated using isolated perfused pancreata of obese and lean male Zucker rats at 12 months of age. 2. In Zucker fatty rats, the insulin secretion rate was significantly (P < 0.01) higher than that of lean rats at all glucose concentrations tested (8.3, 16.7 and 1.4 mmol/l). However, the integrated insulin secretory response to raising the glucose concentration from 8.3 to 16.7 mmol/l was almost absent in these rats. The glucagon secretion rates were significantly lower at 8.3 and 1.4 mmol/l glucose (P < 0.001 for both), and in responses to 10 micrograms/ml tyramine and 0.1 mumol/l noradrenaline (P < 0.05 for both), in Zucker fatty rats. Integrated insulin and glucagon responses to 10 mmol/l arginine were identical in the two groups. 3. Histopathological and immunochemical studies revealed hyperplasia of beta-cells and scattered alpha-cells in the enlarged islets of Zucker fatty rats. 4. These results suggest that, in Zucker fatty rats, the decreased glucagon secretion in the isolated perfused pancreas is attributable to changes in the environment of alpha-cells and/or the inhibitory effects of hypersecreted insulin.

Animals↗
PubMed2000

Biogenic amine formation and oxidation by Staphylococcus xylosus strains from artisanal fermented sausages.

Fifty strains of Staph. xylosus, isolated from artisanal fermented sausages in Southern Italy (Lucania region) were tested to verify their potential to produce or degrade biogenic amines. Twenty-six strains analysed were not able to form amines, but seven had the potential to produce spermine and/or spermidine and, at lower levels, tryptamine and tyramine. By contrast, about 80% of the strains that did not possess amino acid decarboxylase activity, exhibited an ability to degrade histamine. The greatest histamine-oxidase activity was present in the strains S81 (100% degradation), S206 (93%), S79 (68%) and S90 (53%). The strain S142 exhibited a remarkably high potential to oxidase tyramine and histamine, reducing the initial concentrations by 63 and 47%, respectively.

Amine Oxidase (Copper-Containing)↗
PubMed2003

Experimental production of gastric dilation and its association with osmoregulatory stress and biogenic amines in chinook salmon, Oncorhynchus tshawytscha (Walbaum).

Chinook salmon smolt in fresh water fed a commercial diet known to produce minimal gastric dilation and air sacculitis (GDAS) were randomly assigned to four experimental tanks with flow-through sea water. All four groups were acclimatized to sea water for 3 weeks and fed a diet of minced fresh seafood. After 3 weeks the groups were fed either; seafood as before, a different commercial pelleted diet associated with the development of GDAS on farms, or either diet supplemented with 500 mg L(-1) putrescine, 300 mg L(-1) cadaverine and 250 mg L(-1) tyramine. Gastric dilation was produced in fish fed the commercial diet for 1 month but not by feeding a diet of minced seafood. The addition of putrescine, cadaverine and tyramine to either diet had no significant effect on the development of gastric dilation. Fish fed the commercial diet had significantly (P < 0.0001) wider weight-adjusted stomach widths, less prominent longitudinal stomach folds (P < 0.0001) and lower (P < 0.0001) stomach-width ratios than fish fed the fresh seafood diet. There was no significant difference in serum osmolality or sodium concentration between fish from groups with or without gastric dilation or fed biogenic amines.

Air Sacs↗
PubMed1988

Dysfunction of the sympathetic nervous system in cluster headache.

Ocular sympathetic function was studied in 13 cluster headache patients during and between attacks and several weeks or months after attacks had subsided. The pupillary response to tyramine eyedrops and facial sweating and flushing in response to body heating and to the taste of chilies were also investigated during remission. Pupillary dilatation lag on the symptomatic side persisted between bouts and correlated significantly with loss of thermoregulatory sweating in the lower part of the forehead. In six patients in remission, pupillary dilatation in response to tyramine eyedrops was impaired on the symptomatic side, whereas five patients showed no sign of ocular sympathetic deficit. These findings indicate that incomplete sympathetic deficit persisted on the symptomatic side in a subgroup of cluster headache patients during remission. In most of this subgroup the pattern of sympathetic deficit was consistent with impaired function of postganglionic cervical sympathetic fibres.

Adult↗
PubMed1990

Hemicrania continua. The first Spanish case: a case report.

The case of a patient suffering from strictly unilateral continuous headache, absolutely responsive to indomethacin is reported. This is the first Hemicrania continua case to be documented in Spain. The tyramine test resulted in anisocoria with the smaller pupil on the symptomatic side. A second tyramine test after one week on 75 mg indomethacin per day failed to produce anisocoria. Treatment was reduced to 25 mg indomethacin per day, and this dose was sufficient to control the headache completely.

Adult↗
PubMed1999

Effects of serine mutations in transmembrane domain 7 of the human norepinephrine transporter on substrate binding and transport.

Two serine residues in the beta-adrenergic receptor (beta-AR) have been proposed to form hydrogen bonds with the catechol moiety of the ligand and contribute to the activation of the receptor. These conserved serine residues in the dopamine (DA) and norepinephrine transporters (DAT and NET, respectively) have also been shown to affect substrate transport in the rat DAT. In the present work, hydrogen bonding interactions between the corresponding serine residues in the human NET (hNET), 354 and 357, and the hydroxyl groups on the substrate were systematically evaluated by examining the transport and binding properties of DA and several single hydroxyl analogues of DA at wild-type and serine-to-alanine-substituted transporters. A comparison of [3H]nisoxetine binding at the serine 354 mutant, in which K(D) increased 70-fold from the wild-type value, with the binding of DA, m-tyramine (m-TYR), and p-tyramine (p-TYR) at mutant 354, where the increase in Ki was less dramatic, revealed that serine 354 is more influential in inhibitor than substrate binding. The binding of m-TYR and p-TYR at the serine 354 and serine 357 mutants did not show a direct interaction between one serine and one substrate catechol hydroxyl group. DA, m-TYR, and p-TYR binding affinity did not deviate from the wild-type value at the serine 357 and double mutant transporters. At these two transporters, however, the Km of DA uptake increased, suggesting that the roles of serine 357 and serine 354 in substrate transport are different from their roles in binding. The K'm for induced efflux of DA decreased at the serine 357 mutant compared with the wild-type, whereas the K'm at the serine 354 mutant was the same as that of the wild-type. Further investigation of the role of substrate hydroxyls in the transport process revealed no difference between the transport of m-TYR or p-TYR, as measured indirectly through their induced efflux of DA, at any of the mutants. Although these serines are influential in inhibitor and substrate binding to the transporter and substrate uptake and efflux, they do not appear to be involved in a direct hydrogen bond interaction with substrate, suggesting that the pattern of distinct hydrogen bonding interactions at the beta-AR does not exist at the hNET.

Animals↗