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At least 37 records · Page 2Linked to original sources
PubMed1996

Effect of N-feruloyl tyramine (an analogue of tyramine) on inwardly rectifying potassium channel in frog ventricular myocytes.

Electrophysiological effects of N-feruloyl tyramine (NFT), an analogue of tyramine, on potassium currents in frog ventricular myocytes were examined using single-channel recording and whole-cell voltage clamp technique. Extracellular application of NFT induced a concentration-dependent decrease of macroscopic inward rectifier potassium current (iK1) with ID50 of 198 microM, while tyramine (100 microM) was ineffective in producing an inhibitory effect on iK1. NFT reduced the mean open time of iK1 to 1.3 ms from 3.1 ms in control without affecting the amplitude of single-channel conductance. It is indicated that boi containing NFT produces a prolongation of the plateau phase caused by the suppression of inwardly rectifying K channel. Thus, this prolongation may induce an increase in the inflow of Ca ions, which in turn leads to a positive inotropic effect.

Animals↗
PubMed1988

Selective inhibition by 4,alpha-dimethyl-m-tyramine (H77/77) and 4-methyl-alpha-ethyl-m-tyramine (H75/12) of the monoamine oxidase within serotonergic and noradrenergic neurons in the rat brain.

1. The inhibition of monoamine oxidase (MAO) by 4, alpha-dimethyl-m-tyramine (H77/77) and 4-methyl-alpha-ethyl-m-tyramine (H75/12), two amine releasing compounds, within monoaminergic neurons in the rat hypothalamus and striatum in vivo was determined. This was performed by measuring the protection of MAO by the test compound against the irreversible inhibition produced by phenelzine. The MAO activity inside and outside monoaminergic synaptosomes in homogenates of brain tissue was measured in the absence and presence of selective uptake inhibitors at low concentrations of 14C-labelled 5-hydroxytryptamine, noradrenaline or dopamine. 2. It was found that H77/77 and H75/12 produced a pronounced protection against phenelzine within the serotonergic and noradrenergic neurons, whereas much less effect was observed outside these neurons. 3. It was shown that the protection by H75/12 within the serotonergic neurons was somewhat reduced in 5-HT depleted reserpinized rats and that the protection outside these neurons was abolished. Some of the protection of MAO might therefore have been brought about by 5-HT molecules released by H75/12. 4. The marked inhibition of MAO within serotonergic and noradrenergic neurons was counteracted by amine uptake inhibitors and is accordingly brought about by the high concentrations of the accumulated compounds. 5. In contrast to other neuron selective MAO inhibitors, H75/12 decreased the 5-HT concentration in the hypothalamus showing that the releasing effect dominated over the MAO inhibitory effect.

Amphetamines↗
PubMed1993

Preparation of [1-11C]dopamine, [1-11C]p-tyramine and [1-11C]m-tyramine. Autoradiography and PET examination of [1-11C]dopamine in primates.

A method for no-carrier-added 1-11C-labelling of 3-hydroxy-, 4-hydroxy- and 3,4-dihydroxy-substituted phenethylamines is described. [11C]Dopamine, [11C]p-tyramine and [11C]m-tyramine were prepared from on-line produced [11C]nitromethane. Condensation of [11C]nitromethane with various protected and unprotected benzaldehydes was investigated. A one-pot two-step reduction of the substituted 11C-labelled nitrostyrene intermediates, gave after hydrolysis and reversed-phase semi-preparative HPLC-purification the corresponding labelled amines in a total radiochemical yield of 8-20% (based on [11C]CO2 and decay-corrected). The total synthesis time was 45-50 min with a specific radioactivity of 400-1000 Ci/mmol (15-37 GBq/mumol). The radiochemical purity was higher than 98% [11C]Dopamine was used for in vitro autoradiography on human post-mortem brain sections and for positron emission tomography (PET) on Cynomolgus monkeys. Autoradiographic examination of [11C]dopamine binding on human brain section post-mortem demonstrated specific binding in the caudate putamen and the substantia nigra, regions with a dense dopaminergic innervation. Some binding was also seen in the globus pallidum, nucleus ventralis of the thalamus and in nucleus dentatus of the cerebellum, regions where the dopaminergic innervation is very low. In PET examinations of [11C]dopamine binding in Cynomolgus monkeys there was a high uptake of radioactivity in the pituitary, the kidneys and the heart. Any passage of [11C]dopamine across the blood-brain barrier could not be demonstrated. In human PET studies [11C]dopamine has potential as a radioligand for examination of the myocardium, pituitary and kidneys.

Animals↗
PubMed2004

Amino acid residues involved in interaction with tyramine in the Bombyx mori tyramine receptor.

To identify amino acid residues interacting with tyramine (TA) in the Bombyx mori TA (BmTA) receptor, several mutant receptors were expressed in HEK-293 cells and examined for their abilities to bind TA and to attenuate forskolin-stimulated cAMP production in response to TA. The D134A BmTA receptor showed no specific [3H]TA binding and no TA-attenuation of cAMP levels. Although the S218A and S222A BmTA receptors showed no specific [3H]TA binding, they still had the ability to mediate the attenuation of cAMP levels in response to the high concentration (100 microM) of TA. The double mutation of Ser218 and Ser222 to Ala, however, led to the loss of TA-attenuation of cAMP levels. The present study thus confirms that at least three amino acid residues play key roles in interaction with TA in the BmTA receptor.

Amino Acid Sequence↗
PubMed1977

Studies of the fate of tyramine in dogs: the effect of monoamine oxidase inhibition, portafemoral shunt and coronary artery ligation on the kinetics of tyramine.

Radioimmunoassay of tyramine (T) was used to investigate the kinetics of T in plasma of three groups of dogs (control, pretreated with monoamine oxidase inhibitor and those with portafemoral shunt). Furthermore, the influence of coronary artery ligation on the T content of the heart was studied. After i.v. administration of T-HCl (1.7mumol/kg, 0.3 mg/kg), there was a rapid initial decline in T plasma levels with an average T 1/2 of 4.3 minutes. Similar results were obtained in experiments in which the same dose of T-3H was used. There was a 10-fold difference between 3H and T concentrations. Pretreatment with a monoamine oxidase inhibitor resulted in a decrease in T metabolism as reflected by changes in pharmacokinetic parameters (estimated area under the curve AUC, 8166 vs. 1000 ng x min x ml-1, P less than .001; total body clearance, BC, 35.7 vs. 285 ml/min/kg. P less than .005). Similar results were obtained in dogs with portafemoral shunt. Coronary artery ligation resulted in an increase in the level of T in the infarction [1.2. +/- 0.3 (S.E.M.) ng/ml] compared to those of adult volunteers.

Adult↗
PubMed1982

The in vitro release of endogenous m-tyramine, p-tyramine and dopamine from rat striatum.

Administration of phenelzine (100 mg/kg. i.p., 18 hr) increased rat striatal concentrations of pTA, mTA and DA by 30, 6.7 and 1.5 fold, respectively. Lesions of the medial forebrain bundle prevented these increases, permitting the conclusion that the phenelzine-induced amine increases were localized in the synaptic terminals. The release of endogenous pTA, mTA and DA from striatal slices obtained from phenelzine-treated rats was investigated, 50 mM KC1l elicited releases of pTA, mTA and DA which were significantly greater than their respective basal releases. These K+-stimulated releases were antagonized significantly by 15 mM MgCl2, suggesting that they are calcium-dependent in nature. We have concluded, therefore, that mTA and pTA, as well as DA, are released from striatal nerve terminals in vivo. The total amounts of mTA and DA, but not pTA, released in the release experiments were greater than those found in the nonincubated tissue. It appears, therefore, that the biosynthesis of mTA and DA was stimulated during the incubation of the striatal slices.

Animals↗