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PubMed1990

The kinetics of monoamine oxidase inhibition by three 2-indolylmethylamine derivatives.

The inhibition of bovine brain mitochondrial MAO-A and MAO-B by three acetylenic and non-acetylenic derivatives of 2-indolylmethylamine, chosen among more than 100 new compounds, were studied. The non-acetylenic derivative N-methyl-2(5-hydroxy-1-methylindolyl)methylamine (1) was a weak non-selective inhibitor which was shown to act in a reversible and competitive manner towards the deamination of tyramine. The two acetylenic derivatives N-methyl-N-(2-propynyl)-2-(5-benzyloxy-1-methylindolyl)methylamine (2) and N-methyl-N-(2-propynyl)-2-(5-hydroxy-1-methylindolyl)methylamine (3) were potent MAO inhibitors, one of them non-selective (compound 2) and the other MAO-A selective inhibitor (compound 3). Both of them were irreversible and competitive inhibitors, compound 2 towards the deamination of tyramine and compound 3 towards the deamination of serotonin and beta-phenylethylamine. A mechanism for the inhibition of the enzyme by both irreversible inhibitors is proposed and the inhibition parameters are determined.

Alkynes↗
PubMed1975

Studies of suspected neurotransmitters in the vestibuloocular pathways.

Isolated fresh cat trochlear and oculomotor nuclei, which contain the axon terminals of inhibitory neurons whose cell bodies are in the superior vestibular nucleus (SVN), actively synthesize and store [3H]GABA, [14C]acetylcholine, [3H]dopamine and [3H]tyramine from labeled precursors of these compounds. Twelve to 14 days following lesions of the ipsilateral superior vestibular nucleus or its efferent pathway to the oculomotor and trochlear nuclei, at a time when there is extensive degeneration of superior vestibular nucleus axon terminals in these nuclei, the synthesis and storage of GABA in the ipsilateral trochlear nucleus is markedly reduced compared to that in the contralateral trochlear nucleus; the synthesis of acetylcholine, dopamine and tyramine is not measurably affected. The oculomotor nuclei, which unlike the trochlear nuclei receive a heavy bilateral projection from the SVN, show no asymmetric decrease after SVN lesions in their ability to synthesize any of the compounds tested. The data support the identity of GABA as an inhibitory transmitter in the superior vestibular nucleus-trochlear nucleus pathway.

Acetylcholine↗
PubMed1985

Release of endogenous brain epinephrine by the calcium ionophores X537A and A23187.

The Ca2+ ionophores X537A and A23187 produced dose-dependent release of endogenous epinephrine (Epi) as well as norepinephrine (NE) and dopamine (DA) from chopped rat hypothalamus and brainstem. The X537A-induced release of these catecholamines (CAs) was found to be Ca2+-independent, whereas the A23187-induced release was Ca2+-dependent. X537A and A23187 were approximately equipotent in causing the release of the hypothalamic Epi, NE and DA, but X537A was much more effective than A23187 in causing the maximal release. X537A, but not A23187, reduced the total endogenous CA content and increased the total 3,4-dihydroxyphenylacetic acid (DOPAC) content in the chopped hypothalamus. Ca2+-independent release of Epi, NE and DA in the chopped hypothalamus was also observed with indirectly acting sympathomimetic amines (e.g. tyramine and amphetamine). Tyramine and amphetamine did not affect the total endogenous CA contents nor the total DOPAC content. These results suggest that X537A caused release of endogenous brain Epi, NE and DA by transporting the biogenic amines across vesicular or intracellular storage sites. However, A23187 caused release of these CAs by exocytosis via transport of Ca2+ into the neurons.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1978

The effect of urinary pH and flow rate on monoamine output.

Three-hour urinary output values of dopamine, noradrenaline, adrenaline, 2-phenylethylamine and p-tyramine were measured in normal volunteers who had been induced, by pretreatment with ammonium chloride or sodium bicarbonate, to excrete maximally acid or alkaline urine. There were significant effects on the excretion of dopamine, adrenaline and 2-phenylethylamine, inversely proportional to urinary pH value. Adrenaline output increased with increasing urinary flow rate. There was a significant correlation between urinary concentrations of 2-phenylethylamine and p-tyramine. These findings may have important clinical implications.

Biogenic Amines↗
PubMed1982

Platelet monoamine oxidase activity and plasma levels of non-catecholic phenylethylamines in insulin-dependent diabetic subjects.

The activity of blood platelets monoamine oxidase (MAO) was significantly reduced in a group of insulin-dependent diabetics when compared to sex- and age-matched controls. This enzymatic change was accompanied by a dramatic increase in the plasma levels of phenylethylamine, whereas no significant changes were observed for the concentration of either p-tyramine or phenylethanolamine. Levels of the o- and m-isomers of tyramine were below detectable limits (less than 0.050 ng/ml). A possible role of the MAO/monoamine system in the pathophysiology of diabetes is discussed.

Blood Platelets↗
PubMed1992

Cholinesterases exhibiting aryl acylamidase activity in human amniotic fluid.

Acetylcholinesterase (EC 3.1.1.7) and butyrylcholinesterase (EC 3.1.1.8) in human amniotic fluid were estimated in the presence of selective inhibitors. Amniotic fluid cholinesterases (mixture of acetylcholinesterase and butyrylcholinesterase) purified by procainamide-Sepharose affinity chromatography exhibited aryl acylamidase activity which was sensitive to serotonin inhibition (a property of aryl acylamidases associated with both acetyl- and butyrylcholinesterases) and tyramine activation (shown exclusively by aryl acylamidase associated with butyrylcholinesterase). Tyramine activation was unaffected in the presence of the selective acetylcholinesterase inhibitor BW284C51 whereas it was abolished in the presence of the selective butyrylcholinesterase inhibitor ethopropazine, suggesting the presence of both types of aryl acylamidases in amniotic fluid, one associated with acetylcholinesterase and the other associated with butyrylcholinesterase. Butyrylcholinesterase and the associated aryl acylamidase activity in the affinity purified enzyme was selectively immunoprecipitated by a polyclonal antibody raised against human serum butyrylcholinesterase. Estimation of the activity ratio of acetylcholinesterase to butyrylcholinesterase in a few samples of amniotic fluid showed that this could vary depending on the butyrylcholinesterase arising from contaminating blood in the samples. Gel electrophoresis under non-denaturing conditions and enzyme staining showed that butyrylcholinesterase band was detectable on the gel in all the samples whereas acetylcholinesterase band was below detectable levels in normal samples but visible in samples from pregnancies of neural tube defect fetuses. It is suggested that the use of selective cholinesterase inhibitors along with gel electrophoresis and immunoprecipitation studies may be useful in the assessment of cholinesterase activities in human amniotic fluid.

Acetylcholinesterase↗
PubMed1975

The effect of catecholamine depletion on the bradykinin-induced relaxation of isolated smooth muscle.

The effect of depletion of catecholamines by tyramine or reserpine on the bradykinin-induced relaxation of the rat duodenum aan rabbit ileum was the object of this study. The relaxation was not affected by catecholamine depletion due to repeated addition of tyramine to the isolated organs from either normal or reserpine-treated animals. From these findings and on the basis of other data in the literature it can be concluded that the bradykinin relaxation is not due to a release of catecholamines, but rather to a direct effect on the smooth muscle cells.

Animals↗
PubMed1976

Uptake and release of catecholamines in sympathetic nerve fibers in the spleen of the cod, Gadus morhua.

The effects of denervation or pretreatment with reserpine or 6-hydroxydopamine on the contractile responses of the cod spleen have been studied. The contraction produced by tyramine is abolished by pretreatment with reserpine or 6-hydroxydopamine and by denervation. The response to tyramine is restored in reserpine-treated strips after exposure to noradrenaline, but this is not the denervated or 6-hydroxydopamine-treated strips. The response to noradrenaline is potentiated by 6-hydroxydopamine treatment or denervation, while neither acute (2 days) nor chronic (8 days) reserpine treatment have any detectable effect. The effects of 6-hydroxydopamine and denervation are probably due to specific supersensitivity caused by the loss of the presynaptic uptake mechanisms on destruction of the nerve terminals, but contribution by a non-specific postsynaptic supersensitivity is not completely excluded. The effect of acetylcholine is also significantly potentiated by pretreatment with 6-hydroxydopamine or denervation, but not by reserpine, while the dose-response curve for carbachol is not affected by the specific cholinesterase inhibitor BW 284 C51, denervation or 6-hydroxydopamine. The degree of potentiation of the acetylcholine curve caused by both denervation and 6-hydroxydopamine treatment is very similar to that produced by BW 284 C51. It is concluded therefore, that the cholinesterase is associated with nerve fibres which are destroyed by denervation and 6-hydroxydopamine. Although the cod spleen receives both cholinergic and adrenergic sympathetic innervation all responses to nerve stimulation of the perfused spleen are abolished after 6-hydroxydopamine treatment. The possibility is suggested that the sympathetic fibres to the cod spleen represent a primitive type of neuron, with both catecholamines and acetylcholine present within the same terminals.

Acetylcholine↗
PubMed1977

Modulation by histamine of the efflux of radiolabeled catecholamines from rat brain slices.

Histamine induced a dose-dependent stimulation of 3H-catecholamine(CA) efflux (superfusion procedure) from hypothalamic, striatal, hippocampal and cortical slices. The extra-hypothalamic regions were the most sensitive to histamine. Efflux of 14C-GABA and 14C-(acetyl)choline was not affected. The effect of histamine on 3H-CA efflux developed slowly, reaching its maximum after 15-20 min. Histamine was inefffective with tissue from reserpinized animals. The major part of the radioactivity released by histamine consisted of CA metabolites. Histamine apparently does not enter catecholaminergic neurons, since tyramine and the CA had no effect on the efflux of 3H-histamine previously taken up by brain slices. After incubation of slices with 3H-CA in the presence of histamine and subsequent superfusion, tyramine or K+ -depolarization induced much less 3H-CA release than from control slices not incubated with histamine. It is suggested that histamine may act as a modulator of presynaptic catecholaminergic processes in the central nervous system by causing a depletion of the transmitter stores in the nerve terminals.

Acetylcholine↗
PubMed1977

Studies on the depletion of brain amines by m-tyrosine.

The biochemical basis of the well-known physiological and pharmacological actions of m-tyrosine was examined by a detailed study of its effect on the brain biogenic amines. m-Tyrosine was injected i.p. and rat brain monoamine levels were measured. Endogenous levels of dopamine, norepinephrine and serotonin all showed approximately 50% reductions 1 h after the administration of L-m-tyrosine at 150 mg/kg. These actions of L-m-tyrosine could be blocked by the inhibition of the central dopa decarboxylase. Depletion of brain monoamines was also observed with the D-isomer of m-tyrosine, although this effect was less pronounced than that of the L-isomer. In vitro experiments with rat brain homogenates showed that L-m-tyrosine, m-tyramine and m-octopamine enhanced in efflux of exogenous labeled monamines from brain particles, whereas D-m-tyrosine was completely ineffective. From these results it is concluded that the observed decreased in brain monamine levels by L-m-tyrosine may be due to a m-tyramine-enhanced release of the amines which are quickly metabolized in vivo.

Animals↗
PubMed1979

Release of radioactive purines from cat nictitating membrane labeled with 3H-adenine.

Cat nictitating membranes were incubated with 1-2 x 10(-7) M 3H-adenine or 3H-adenosine for 1 h. A tissuebath ratio of about 15 was found for both compounds in intact and denervated membranes. In intact nictitating membranes sympathetic nerve stimulation (4 Hz, 5 min) caused a net release of purines (0.66 +/- 17% of the tissue content), which was reduced by alpha-blockade. Noradrenaline (1-3 microM) or tyramine 60 microM), which produced the same contractile response as did nerve stimulation, increased purine release to the same extent as did nerve stimulation. The effect of either agent was reduced or abolished by phentolamine. Purine release could also be induced by acetylcholine and ATP. This release was not altered after surgical denervation. There was an excellent correlation between the contractile response and the purine release induced by nerve stimulation, noradrenaline, tyramine and acetylcholine. However, ATP caused a larger release of 3H-purines than expected from the contractile responses, possibly indicating displacement. The results indicate that most if not all of the 3H-purines released by nerve stimulation in the cat nictitating membrane are derived from postjunctional elements.

Acetylcholine↗
PubMed1984

Reserpine-induced supersensitivity occurs for beta-adrenoceptor-mediated responses of heart and trachea but not of the uterus and lung.

This study was undertaken to determine whether reserpine-induced supersensitivity occurs in tissues containing beta1-adrenoceptors and in those with beta 2-adrenoceptors. Guinea-pigs and rats were pretreated with reserpine for either 3 days (5 mg kg-1 i.p. at 72 h, 3 mg kg-1 at 48 h and 3 mg kg-1 at 24 h before use) or 7 days (1 mg kg-1 daily). The sensitivities of left and right atria, papillary muscles, tracheal spirals, lung strips and uteri to isoprenaline were compared with those from untreated animals. The positive inotropic responses of left atria and papillary muscles and chronotropic responses of right atria from reserpine-pretreated animals were supersensitive to isoprenaline, the concentration-response curves being to the left. The relaxation response of the carbachol-contracted trachea also exhibited supersensitivity, but to a lesser extent. However, no supersensitivity occurred for the relaxation of carbachol-contracted lungs, K+-depolarized guinea-pig uteri or electrically stimulated rat uteri. As a pharmacological index of the presence of releasable noradrenergic stores, tyramine was added cumulatively to each tissue. Only cardiac and tracheal preparations yielded substantial responses, indicating the presence of sympathetic innervation. A relaxation of the rat uterus by tyramine was not attributable to releasable noradrenaline stores. The supersensitivity of the heart and trachea could therefore be associated with their sympathetic innervation and with the fact that their responses are mediated via beta 1-adrenoceptors; the trachea containing a small proportion of beta 1-adrenoceptors. The responses of the lung and uterus, however, are beta 2-adrenoceptor-mediated and failed to exhibit supersensitivity. Since the supersensitivity is a consequence of the neuronal depleting action of reserpine, these results are compatible with the concept that beta 1-adrenoceptors are associated with sympathetic innervation whereas beta 2-adrenoceptors are not.

Animals↗
PubMed1987

Biogenic amines in the Arthus reaction.

The concentrations of serotonin, tryptamine, dopamine, and tyramine were quantitatively determined in the Arthus reaction, since the activity of histamine-N-methyltransferase (HMT), a major histamine-metabolizing enzyme that had been demonstrated to be inhibited by such biogenic amines in vitro, decreased significantly in the reaction site. The concentrations of serotonin, tryptamine, and dopamine were unchanged in dinitrochlorobenzene allergic and croton oil dermatitis except for a slight increase of tryptamine in the latter. Tyramine was unable to be demonstrated quantitatively in all specimens tested. The concentration of serotonin decreased to about 30% that of the control level until 1 hr, followed by a prominent increase to about two-fold at 6 hr after the initiation of the Arthus reaction accompanying with a concomitant decrease in HMT activity. However, the concentrations of tryptamine and dopamine were rather decreased in the reaction site, and the net decrease of two amines was far greater than the increased amount of serotonin. The decrease in HMT activity is not stoichiometrically well elucidated from these results, and therefore, the presence of other hypothetic inhibitory factors that are increased in the Arthus reaction should be suspected.

Animals↗
PubMed1985

Intracellular transport of asialoglycoproteins in rat hepatocytes. Evidence for two subpopulations of lysosomes.

The intracellular transport and degradation of asialoorosomucoid (AOM) in isolated rat hepatocytes was studied by means of subcellular fractionation in Nycodenz gradients. The asialoglycoprotein was labelled by covalent attachment of a radioiodinated tyramine-cellobiose adduct ( [125I]TC) which leads to labelled degradation products being trapped intracellularly and thus serving as markers for the degradative organelles. The ligand was initially (1 min) in a slowly sedimenting (small) vesicle and subsequently in larger endosomes. Acid-soluble, radioactive degradation products were first found in a relatively light lysosome whose distribution coincided in the gradient with that of the larger endosome. Later (30 min) degradation products were found in denser lysosomes which banded in the same region of the gradient as the lysosomal enzyme, beta-acetylglucosaminidase. Colchicine, monensin and leupeptin all inhibited degradation of [125I]tyramine-cellobiose asialoorosomucoid ( [125I]TC-AOM) and reduced the formation of degradation products in both the light and the dense lysosomes. In presence of monensin and colchicine no undegraded ligand was seen in the dense lysosome, suggesting that uptake in these vesicles was inhibited. Leupeptin allowed accumulation of undegraded ligand in the dense lysosome. Therefore, transfer from light to dense lysosomes is not dependent on degradation as such. In the presence of monensin two peaks of undegraded ligand were found in the gradients. It seems possible that in the monensin-sensitive endosomes, dissociation of the ligand-receptor complex is inhibited, allowing ligand to recycle with the receptors in small vesicles.

Animals↗
PubMed1989

Vascular responses of ophthalmic arteries to exogenous and endogenous norepinephrine.

A participation of neuronal and tissue uptake mechanism in responses to periarterial electrical sympathetic nerve stimulation (ES) and intra-arterial applications of norepinephrine (NE) was investigated in the isolated and perfused canine ophthalmic arteries (OA), using key pharmacological drugs such as imipramine, tyramine, cocaine, cortisol and diltiazem. Results were as follows: (1) NE, KCl and ES induced marked vasoconstrictions in a dose- and frequency-related manner, but tyramine induced only a slight constriction even at large doses; (2) cortisol, an uptake2 blocker, did not significantly modify KCl- and ES-induced vasoconstrictions, but significantly enhanced NE-induced responses; (3) small doses of imipramine, a neuronal uptake1 blocker, did not modify NE-induced vasoconstrictions, but large doses decreased them. On the other hand, the ES-induced response was slightly increased by a relative small dose of imipramine; (4) cocaine, another uptake1 blocker, slightly enhanced NE- and ES-induced responses; (5) ES-induced response was reduced by not only diltiazem, but also Ca2+-free solution with EGTA (1 mM l-1). The NE-induced response was not affected by diltiazem (Ohkubo and Chiba, 1987, Exp. Eye Res. 45, 263-70), and slightly but significantly depressed by Ca2+-free solution with EGTA. These results suggest that tissue and neuronal uptake mechanisms exist in responses to ES and NE1, the response to ES was markedly dependent on Ca2+ influx to the cell membrane2, and exogenous NE may induce Ca2+ movement mainly from the intracellular store site.

Animals↗
PubMed1985

Vascular monoamine oxidase activity in the rat brain: variation with the substrate and the vascular segment.

Brain vascular monoamine oxidase (MAO) was assayed in order to determine (a) whether microvessel MAO is more or less specific for certain substrates and (b) if the extraparenchymal, pial arteries possess an MAO activity as high as that in the microvessels. Rat brain microvessels were prepared by gentle homogenisation of grey matter, followed by filtration and differential centrifugation of the matter retained. Pial arteries were carefully freed of the meninges and cut into small segments. For comparison, rat mesenteric arteries were also dissected out and cut up. MAO was assayed by measuring the rate of oxygen consumption in a small cell with a Clark electrode. Although a high microvessel MAO activity (2.2 +/- 0.3 nmol min-1 mg prot.-1) was found using noradrenaline as substrate, significantly higher rates were found with tyramine, serotonin and beta-phenyl-ethylamine. By contrast, both pial and mesenteric arteries showed a 6-7 fold lower activity (substrate tyramine). These results indicate first, that a certain specialisation of the microvessel MAO activity exists which is apparently independent of the classical A or B-form category of the substrates, and second, that the extraparenchymal vessels (pial arteries) appear to possess significantly lower MAO activity, in accordance with the concept that blood-brain properties are induced by the cerebral parenchyma.

Animals↗
PubMed1989

Release of some endogenous trace amines from rat striatal slices in the presence and absence of a monoamine oxidase inhibitor.

The basal and 50 mM K+-stimulated release of m-tyramine (mTA), p-tyramine (pTA), tryptamine (TR) and phenylethylamine (PE) from striatal slices obtained from rats pretreated with a monoamine oxidase inhibitor (MAOI) was investigated. A K+-stimulated release of mTA and pTA was observed, but K+ did not stimulate either TR or PE release. The latter two amines, therefore, are unlikely to be conventional neurotransmitters in the rat striatum. The release of endogenous striatal pTA from control rats was also investigated. Veratridine stimulated endogenous pTA release, but 50 mM K+ did not. It is possible, therefore, that endogenous pTA can be released in a transmitter-like fashion.

Animals↗
PubMed1996

Norepinephrine release during vasoconstriction induced by cross-linked hemoglobin.

The pressor effect of hemoglobin-based blood substitutes is due partly to their capacity to scavenge nitric oxide (NO), a potent vasodilator. NO also appears to modulate the release of norepinephrine (NE) from sympathetic nerve endings in some blood vessels. Thus studies were designed to determine if contraction occurring in response to alpha alpha-cross-linked hemoglobin (XL-Hb) is due in part to increased exit of NE from vascular nerve endings. Helical strips of canine femoral artery were superfused in vitro with Krebs-Ringer solution and, for each strip, the overflow of NE into the superfusate as well as contractile responses were measured concurrently during basal conditions, during nerve stimulation and during tyramine-evoked release of NE. XL-Hb (10 microM) contracted unstimulated strips without affecting NE overflow. NE overflow also was unchanged by NG-monomethyl-L-arginine (L-NMMA; 300 microM), an inhibitor of NO synthesis; by sodium nitroprusside (SNP; 1 microM) an NO donor; by a combination of XL-Hb and L-NMMA; or of XL-Hb and SNP. These treatments contracted the strips to the same degree as did XL-Hb alone, except for SNP, which induced relaxation. Transmural stimulation of the strips at 2 and 10 Hz induced NE overflow and contraction, neither of which was affected by any treatment except SNP which significantly (P < 0.05) increased NE overflow while inhibiting contraction. In other experiments, XL-Hb augmented contractions induced by tyramine (10 microM) although the resulting NE release was unaffected. These results suggest that, in the femoral artery, contractions induced by XL-Hb are not due to increased efflux of NE from vascular nerve endings but are consistent with inhibition of the the actions of NO.

Animals↗