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PubMed1984

Vasoconstrictor responses of isolated and perfused canine mesenteric arteries to alpha-adrenoceptor agonists.

Using isolated and perfused canine mesenteric artery, vasoconstrictor responses to alpha-adrenoceptor stimulating agents were compared. The order of potencies for inducing vasoconstriction was epinephrine greater than norepinephrine greater than phenylephrine greater than methoxamine greater than dopamine much greater than tyramine greater than clonidine greater than or equal to xylazine. A selective alpha 2-stimulant, xylazine, did not induce any significant vasoconstrictor response. Tyramine produced only a slight vasoconstriction. Responses to norepinephrine, phenylephrine and methoxamine were competitively inhibited by phentolamine treatment. From these results, it is concluded that the adrenoceptor in the canine mesenteric artery may be characterized as an alpha 1-receptor and that release of norepinephrine by tyramine is not marked in this relatively large vessel.

Adrenergic alpha-Agonists↗
PubMed1984

Fasting reduces the responses of the rat vas deferens to sympathomimetics.

The effect of fasting, L-DOPA pretreatment and high glucose medium on the response of the rat vas deferens to sympathomimetics was studied in vitro. The contractile responses of the rat isolated vas deferens were reduced by fasting, the effect being significant after 24-hr fast with noradrenaline and tyramine, after a 48-hr fast with dopamine, and after a 72-hr fast with methoxamine. Treatment with L-DOPA for 7 days before sacrifice abolished the effect of a 24-hr fast in reducing responses to noradrenaline and tyramine, and the response to methoxamine after a 72-hr fast was enhanced. Doubling the concentration of glucose in the solution bathing the isolated vas deferens from rats fasted for 24 hr increased the responses to noradrenaline and tyramine. It is concluded that fasting reduces the responses of the rat vas deferens to sympathomimetics whilst L-DOPA pretreatment and high glucose restore and/or enhance the responses.

Animals↗
PubMed1982

Correlation between noradrenaline fluxes, metabolism and compartmentalisation in human platelets.

(3H) noradrenaline was taken up by human platelets and partially converted into sulfoconjugated noradrenaline. This uptake was inhibited by drugs which have been previously shown to impair the uptake of 5-HT (ouabain, chlorimipramine) or the storage of 5-HT (tyramine, reserpine) by platelets. In addition, tyramine and reserpine stimulated the formation of sulfoconjugated noradrenaline. The efflux of noradrenaline from platelets was measured in parallel and was found to be directly related to the proportion of non metabolized to metabolized noradrenaline in the cells. Unlike tyramine, which induced a similar release of noradrenaline and 5-HT, reserpine was less effective at inducing noradrenaline release than 5-HT release. This study indicates a preferential localization of noradrenaline in the granular pool of human platelets with the existence of an extragranular sulfoconjugated pool which is increased when the granular storage of noradrenaline is impaired. Studies of noradrenaline fluxes and metabolism may be useful in the understanding of both acquired and inherited platelet storage pool defects.

Blood Platelets↗
PubMed1978

Mechanism of positive chronotropic response of the canine SA node to selective administration of ketamine.

Mechanism for induction of the positive chronotropic effect of ketamine was studied in vivo using a selective perfusion technique of the canine SA node artery. In the reserpinized dogs in which tyramine responsiveness could be restored with norepinephrine, an injection of ketamine induced no sinus acceleration, while its prior administration to norepinephrine suppressed the response to tyramine. In the tetrodotoxin treated preparation in which the effect of electrical stimulation of the vagus and the stellate ganglion was abolished, tyramine produced an increase of sinus rate as usual, but the induction of sinus tachycardia by cocaine and ketamine was completely blocked. The results indicated that the positive chronotropic response of the SA node to ketamine might be induced by an inhibition of the norepinephrine uptake at the adrenergic nerve endings in a cocaine-like manner.

Animals↗
PubMed1982

Use of rapid superfusion to differentiate the release of dopamine from striatal tissue induced by sympathomimetic amines from release induced by potassium.

A rapid superfusion system incorporating a continuous amperometric detector has been employed to study the effects of p-tyramine, d-amphetamine and cocaine on K+-stimulated release of dopamine (DA) from striatal tissue. Qualitative identification of the released substances is made by liquid chromatography with electrochemical detection and DA is established to be the principal substance released following exposure of the tissue to 60 mM K+ in the presence of Ca++. At a superfusion rate of 1 ml/min with a 20 microliter volume tissue holder, d-amphetamine and p-tyramine do not elicit detectable release of endogenous substances. These results are in direct contrast to the significant release of DA observed when striatal tissue is incubated with d-amphetamine for the same time period and suggest that the pools susceptible to release by the sympathomimetic amines are removed by superfusion. When striatal tissue is superfused with a buffer containing 60 mM K+ and cocaine or sympathomimetic amines, the effects of uptake blockade are manifested as an increase in the amount and duration of observed release over that obtained with 60 mM K+. In a competitive study of cocaine and p-tyramine with d-amphetamine, it appears that all three of these agents induce blockade at the same site(s). All of these data are in direct accord with the facilitated exchange diffusion mechanism proposed for the actions of sympathomimetic amines at DA nerve terminals.

Animals↗
PubMed1994

Immunohistochemical localization of L-dopa and aromatic L-amino acid-decarboxylase in the rat retina.

PURPOSE: The purpose of this study was threefold: to determine if some catecholaminergic amacrine cells of the rat retina use L-DOPA as their neurotransmitter, especially the small (2CA) cells that are immunoreactive to tyrosine hydroxylase but not to dopamine; to understand better the possible existence of serotoninergic cells in the rat retina; and to clarify the role of serotonin in the metabolism of melatonin. METHODS: Immunohistochemistry using antibodies against tyrosine hydroxylase (TH), L-DOPA, aromatic L-amino acid decarboxylase (AADC), dopamine (DA), and tyramine in rat retinal wholemounts, serial sections, and various combinations of double labeling. RESULTS: Paired wholemounts immunoreacted with anti-TH/AADC antibodies did not show a significant difference in densities of TH+ and AADC+ amacrine cells. All the TH+ cells exhibited AADC immunoreactivity. There were no AADC-immunoreactive cells lacking TH. A few TH+ cells exhibited L-DOPA immunoreactivity; they also contained AADC. The inner segments of photoreceptor cells were labeled by the anti-AADC antibody. The antibody to tyramine did not label any cells in the rat retina. CONCLUSIONS: L-DOPA can be excluded as a candidate active substance for the small TH+ amacrine cells that do not exhibit DA-immunoreactivity. The L-DOPA-immunoreactivity restricted to a small number of large TH+ amacrine cells probably does not represent an end product. Tyramine also does not appear to constitute a neurotransmitter in the rat retina. We confirm that there are no serotonin-synthesizing amacrine cells in the rat retina. The localization of AADC-immunoreactivity in the photoreceptor cell inner segments is possibly related to the biosynthetic pathway of melatonin from 5-hydroxytryptophan.

Animals↗
PubMed1993

Clinical pharmacology of reversible monoamine oxidase-A inhibitors.

Traditional monoamine oxidase inhibitors (MAOIs) have long been associated with tyramine-related hypertension--the cheese effect. Despite their undoubted clinical efficacy, this problem has restricted their use. New, selective, and reversible MAO-A inhibitors--which act only on the A isoenzyme--appear not to have this effect. Our investigations of these drugs, exemplified by brofaromine, have shown a reduced and more rapidly reversed tyramine pressor sensitivity. Moreover, we were unable to detect any clinically significant food interaction, following ingestion of a quantity of cheese containing sufficient tyramine to increase systolic blood pressure by at least 30 mm Hg. These results confirm the improved safety of brofaromine, and other drugs in this class, when compared with classic MAOIs.

Blood Pressure↗
PubMed1993

[The amine-forming ability of Aeromonas spp].

Motile Aeromonas (A.) species are considered international more and more as potential food poisoning organisms. Their ability to produce biogenic amines, products of metabolism, which in case can cause a disease, was only searched insufficiently till now. 50 strains of the species A.hydrophila, A.sobria, A.caviae and the non-motile species A.salmonicida were included in the tests for amine producing potency. Qualitative investigations to the formation of histamine, tryptamine, and tyramine were ensued by the help of thin layer chromatography. Quantitative investigations were only done in respect of the production of tyramine, which had been proved qualitatively in several strains, while histamine and tryptamine were not produced. Concentrations of tyramine with foodhygienic relevance were found out partially.

Aeromonas↗
PubMed1977

Inhibition of norepinephrine uptake by phenoxybenzamine and desmethylimipramine in the isolated guinea-pig atrium.

The effects of phenoxybenzamine (PBZ) and desmethylimipramine (DMI) on 3H-norepinephrine uptake by sympathetic nerve terminals of isolated guinea-pig left atrium has been investigated in the absence and in the presence of norepinephrine, tyramine, cocaine and isoproterenol, used as protecting agents. PBZ blocked the uptake of 3H-norepinephrine by 50% at a concentration of 3 micronM. For DMI the ID50 was approximately 0.33 micronM. These doses were used for all subsequent protection experiments. When incubation with PBZ was carried out in the presence of tyramine (574 micronM) the blocking effects of PBZ were completely reversed. In contrast, tyramine was unable to protect against 3H-norepinephrine uptake blockade elicited by DMI. Norepinephrine (20 micronM) or cocaine (29 micronM) afforded no protection against DMI-induced 3H-norepinephrine uptake blockade, but both agents significantly protected against blockade of PBZ. Isoproterenol (40 micronM) was unable to protect against 3H-norepinephrine uptake blockade evoked either by PBZ or DMI. The results provide strong evidence for a different site and/or mechanism of action of PBZ and DMI on the norepinephrine uptake system at adrenergic nerve terminals.

Animals↗
PubMed1976

Regional variation in the distribution of alpha-adrenoreceptors in the vas deferens of the rat.

Experiments were performed with preparations obtained by medial transection of the rat vas deferens. Eight sympathomimetic drugs: noradrenaline, alpha-methylnoradrenaline, phenylephrine, dopamine, tyramine, amphetamine, cocaine and isoprenaline, were applied to preparations which were field-stimulated at 10 sec intervals. On the testicular half of the tissue all except isoprenaline enhanced twitches and/or caused contractions. These effects were blocked by alpha-adrenoreceptor antagonists. On the urethral preparation all except phenylephrine, which often enhanced twitches, inhibited responses to field stimulation. These effects were not blocked by alpha-adrenoreceptor antagonists or by propranolol, though the latter blocked inhibitory effects of isoprenaline on both segments. Inhibitory responses to tyramine persisted in urethral segments treated with cocaine and in urethral segments taken from reserpine-treated rats, and thus tyramine may have some direct action. No regional variation was observed in response to acetylcholine or carbachol. High potassium concentrations were equally effective in contracting both segments, but the time courses of contractions differed. These experiments confirm a density gradient of excitatory alpha-adrenoreceptors along the length of the rat vas deferens.

Adrenergic alpha-Antagonists↗
PubMed1976

Molecular turnover numbers of different forms of mitochondrial monoamine oxidase in rat.

Molecular turnover numbers of the different forms of monoamine oxidase in rat liver were estimated for serotonin, tyramine and beta-phenylethylamine by titration with irreversible inhibitors. The 'A' form was found to have a much higher turnover number for serotonin and a lower turnover number for beta-phenylethylamine than the 'B' form, while the turnover numbers for tyramine were in the same order of magnitude for both forms. The monoamine oxidase in the liver was found to have a significantly higher molecular turnover for tyramine and beta-phenylethylamine than that in the brain, heart and kidney. It was calculated that the 'A' form of monoamine oxidase amounted to about 20% and the 'B' form to about 80% of the total amount of monoamine oxidase in the rat liver mitochondrial preparation. The number of molecules per mitochondrion was also calculated.

Animals↗
PubMed1992

A new specific antibody reveals octopamine-like immunoreactivity in cockroach ventral nerve cord.

An antiserum was raised in rabbits immunized with octopamine conjugated to thyroglobulin. The specificity of this antiserum for octopamine is shown by dot blot immunoassay analysis. The antiserum does not crossreact with dopamine, noradrenaline, and serotonin, but slight crossreactivity with the amine tyramine at high concentrations was observed. The tyramine crossreactivity could be eliminated by preabsorption with a tyramine-glutaraldehyde-BSA conjugate. Using this antiserum, we describe the topographical distribution of octopamine-immunoreactive (ir) neuronal elements in wholemounts and paraffin sections of the ventral nerve cord of the American cockroach. The pattern of octopamine immunostaining is completely different from that obtained with an antidopamine serum, and can be blocked by preabsorbing the antioctopamine serum with BSA-conjugated octopamine. Cell bodies and dendritic processes of putatively octopaminergic dorsal (DUM) and ventral (VUM) unpaired median neurons were clearly octopamine-ir in all ganglia examined. The numbers of stained DUM somata in the mesothoracic, metathoracic, and terminal ganglion of females correspond to those of peripherally projecting DUM cells revealed previously by retrograde tracing (Gregory, Philos Trans R Soc Lond [Biol] 306:191, 1984; Tanaka and Washio, Comp Biochem Physiol 91A:37, 1988; Stoya et al., Zool Jb Physiol 93:75, 1989). In addition, various, previously unknown, paired cells with octopamine-like immunoreactivity were found in all ventral ganglia except abdominal ganglia 3-6. Some of these probably project intersegmentally.

Animals↗
PubMed1993

An examination of the reliability of the radiochemical assay for monoamine oxidases A and B.

The radiochemical assay for MAO A has been compared with the polarographic and alcohol dehydrogenase-coupled assays, using 5-hydroxytryptamine (5-HT) and tyramine and the homogeneous human liver enzyme expressed in yeast, and rat liver mitochondria. Despite efforts to measure true initial rates and to avoid known sources of error in the radiochemical procedure, significantly higher rates (Vmax) and lower Km values for the substrate were obtained with the polarographic than with the radiochemical method for 5-HT and tyramine, using either highly purified enzyme or mitochondria. The rate of tyramine oxidation measured by the polarographic method and the coupled assay agreed well, however. Consequently, for kinetic and inhibition studies we recommend the polarographic method for MAO A substrates. Comparison of the radiochemical, polarographic, spectrophotometric, and coupled assays for MAO B from beef liver (mitochondria and homogeneous enzyme) showed polarography to be the method of choice on all substrates tested, although, if all known sources of error are carefully controlled, the radiochemical assay gives the same Vmax and Km values. We also report that with each substrate studied the apparent Km is much lower when mitochondria are used than when the highly purified, virtually lipid-free preparations of MAO A are studied.

Animals↗
PubMed1979

Brain region differences and some characteristics of monoamine oxidase type A and B activities in the vervet monkey.

Monoamine oxidase in the vervet monkey showed greater variations in activity in six brain regions when tyramine or phenylethylamine was used as the substrate (3.8- to 4.1-fold differences) than when serotonin was the substrate (1.8-fold differences). With phenylethylamine and tyramine as substrates, the highest MAO specific activities were found in the hypothalamus and the lowest in the cerebellum and cortex. With serotonin as the substrate, the highest specific activities were in the mesencephalon and cortex. The inhibition of tyramine deamination by clorgyline and deprenyl yielded biphasic plots indicative of the presence of MAO-A and MAO-B enzyme forms in the vervet brain. On the basis of these inhibitor curves, the vervet brain could be estimated to contain approximately 85% MAO-B and 15% MAO-A, in contrast to rat brain which contains 45% MAO-B and 5% MAO-A. The inhibition of serotonin deamination by deprenyl in vervet brain yielded a biphasic plot, suggesting that some serotonin deamination in the vervet is accomplished by the MAO-B enzyme form. Estimations of the relative amounts of MAO-A and MAO-B based on inhibitor curves or based on substrate ratios yielded proportionate results which were in close agreement across the different brain regions, supporting the validity of these approaches to estimating MAO-A and MAO-B activities.

Animals↗
PubMed1981

Preparation of antibodies to catecholamines and metabolites--syntheses of various immunogens and characterization of the resulting antibodies.

The synthesis of antigens of the haptens p-tyramine, octopamine, synephrine, dopamine, normetanephrine, beta-(3,4-dichlorophenyl)-ethylamine and 3-fluoro-tyramine is described. The coupling of the haptens to the carrier protein was performed either via the side chain by means of succinic anhydride, or through the phenolic ring via an aminomethyl group which was introduced by a Mannich reaction. Antisera to these haptens were produced in rabbits by immunization with these antigens. The antisera were characterized by determination of titer and specificity (p-tyramine, synephrine, normetanephrine). The possibility is discussed of using antisera to p-hydroxyphenylethylamine for a radioimmunological determination of catecholamines.

Animals↗
PubMed1990

Inhibition of sympathetic neurotransmitter release by modulators of cyclic GMP in canine vascular smooth muscle.

The contractile response to neurally released norepinephrine (NE) from sympathetic nerve endings innervating vascular smooth muscle are inhibited by substances which raise either cyclic AMP and cyclic GMP concentrations in smooth muscle. However, cyclic AMP is believed to facilitate NE release from sympathetic nerves whereas the role of cyclic GMP in this process is undefined. We examined the effects of presumed modulation of the intraneuronal concentration of cyclic AMP and cyclic GMP on sympathetic neurotransmission to isolated canine mesenteric artery by measurement of the efflux of [2-14C]NE during transmural nerve stimulation (calcium dependent release of NE) and administration of tyramine (calcium independent release of NE) and measurement of the contractions to exogenous NE and tyramine. Stimulation of adenylate cyclase with forskolin, prostacyclin and iloprost, a stable prostacyclin analog, and inhibition of Type III cyclic AMP phosphodiesterase with neural specific rolipram, 'non-specific pelrinone and milrinone and isobutylmethylxanthine did not enhance the efflux of [2-14C]NE from sympathetic nerves innervating the blood vessels. Isoproterenol enhanced the efflux of [2-14C]NE. The effect was inhibited by propranolol but not affected by milrinone, amrinone or rolipram. Activators of guanylate cyclase (SIN-1a an active metabolic of molsidomine, nitroglycerin and sodium nitroprusside) and inhibitors of Type II cyclic GMP phosphodiesterase (M&B-22948 and verofyllin) inhibited the efflux of NE released by transmural nerve stimulation but not by tyramine. These data support the conclusion that cyclic GMP may be an inhibitory modulator of calcium and depolarization dependent NE release from sympathetic nerves, whereas neuronal cyclic AMP may not be a primary modulator of neurotransmission to vascular smooth muscle.

3',5'-Cyclic-GMP Phosphodiesterases↗
PubMed1985

Radioiodinated ganglioside GM1: a potential tool for the investigation of ganglioside function in vivo.

Ganglioside GM1 was labeled with 125I either directly or after conjugation to tyramine. Direct iodination of the sphingosine chain resulted in a compound which dehalogenated rapidly both in vitro and in vivo. The binding of the 125I[GM1-tyramine] conjugate to neuronal membranes in vitro was similar to that reported for 3H-GM1. The biodistribution of 125I activity after intravenous injection of 0.5 uM and 5 uM 125I[GM1-tyramine] in mice was also similar to that reported for 3H-GM1. This radioiodinated GM1 derivative might be useful for the study of ganglioside GM1 function in vivo.

Animals↗
PubMed1994

Prejunctional action of the venom from the Indian red scorpion Mesobuthus tamulus on adrenergic transmission in vitro.

Venom (RSV) from the Indian red scorpion, Mesobuthus tamulus (Buthus tamulus), can cause increased peripheral sympathetic activity with consequent enhancement of adrenergic responses. We have therefore investigated the effects of RSV on adrenergic transmission in the rat isolated anococcygeus muscle. The effects of phentolamine (5 microM), tetrodotoxin (2 microM), guanethidine (5 microM), desipramine (1 microM) and reserpine pretreatment in vivo (5 mg/kg s.c. x 24 hr and 5 mg/kg i.p. x 3 hr) on the contractile responses of the rat anococcygeus muscle to RSV (1.5 microgram/ml), field stimulation, noradrenaline (NA, 1 microM or 3 microM) and tyramine (15 microM) were compared. The contractile responses to RSV and to field stimulation were completely blocked by phentolamine, tetrodotoxin, guanethidine and reserpine pretreatment, but the responses were potentiated by desipramine. The contractile responses to tyramine were completely blocked by phentolamine, reserpine pretreatment as well as desipramine. The responses to NA were completely blocked by phentolamine, but were potentiated by guanethidine, desipramine and reserpine. Relatively low concentrations (0.1 microgram/ml x 4) of RSV which did not produce any observable increase in tone of the anococcygeus muscle, potentiated the contractile response of the anococcygeus muscle to field stimulation, but not the responses to exogenous NA; 4-aminopyridine (25 microM x 2) also potentiated the muscle responses to field stimulation. HPLC measurements revealed only very low concentrations (0.10 +/- 0.03 mumol/g venom) of NA in RSV. Thus, the adrenergic agonist action of RSV in the rat isolated anococcygeus muscle can be attributed to the involvement of some prejunctional mechanism(s) of action that stimulates the release of neurotransmitter which differs from the indirect action mediated by tyramine.

Animals↗