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PubMed2004

Modification of transmitter release from periarterial nerve terminals by dipyridamole in canine isolated splenic artery.

1. The aim of the present study was to determine the modulatory effects of dipyridamole on purinergic and adrenergic transmission in the canine isolated, perfused splenic artery. 2. Periarterial nerve electrical stimulation readily induced a double-peaked vasoconstriction consisting of an initial transient, predominantly P2X receptor-mediated constriction followed by a prolonged, mainly alpha1-adrenoceptor-mediated response. 3. Exposure of tissues to dipyridamole (0.1-1 micro mol/L) dose-dependently inhibited both the first and second peaks of the vasoconstrictor response at a low frequency of stimulation (1 Hz), whereas at an intermediate frequency of stimulation (4 Hz), the first peak of the response was depressed without any significant effect being observed on the second peak of constriction. 4. At a higher dose (1 micro mol/L) dipyridamole potentiated vasoconstrictor responses to noradrenaline (0.03-1 nmol). At any doses used, dipyridamole had no effect on the vasoconstrictor responses to ATP (0.03-1 micro mol). 5. Tyramine (0.01-0.3 micro mol) induced vasoconstriction in a dose-dependent manner. The dose-response curves for tyramine were shifted to the right following treatment with dipyridamole (0.1-1 micro mol/L). 6. The present results indicate that dipyridamole may inhibit purinergic and adrenergic transmission presynaptically, whereas postsynaptically dipyridamole may potentiate the adrenergic vascular constriction by inhibition of transmitter uptake.

Adenosine Triphosphate↗
PubMed1981

Biosynthesis of N-acetyldopamine and N-acetyloctopamine by Schistocerca gregaria nervous tissue.

N-Acetyltyramine, N-acetyldopamine and N-acetyloctopamine were the major products when either L-[3H]tyrosine or [3H]tyramine were incubated with thoracic ganglia of the desert locust, Schistocerca gregaria. No label was incorporated into L-DOPA under these conditions, although 2-3% of the radioactivity could be recovered in dopamine and octopamine. Addition of the aromatic amino acid decarboxylase inhibitor, 3-hydroxybenzylhydrazine (NSD 1015), prevented the formation of N-acetylcompounds from L-[3H]tyrosine, without resulting in an accumulation of label in L-DOPA. In contrast, incubation of samples of haemolymph with L-[3H]tyrosine resulted in the recovery of 7% of label in L-DOPA, which was increased to 17% in the presence of NSD 1015. These results provide evidence that the initial step in the synthesis of dopamine and octopamine by S. gregaria nervous tissue is the conversion of L-tyrosine to tyramine, which is subsequently metabolised to N-acetyltyramine, N-acetyldopamine or N-acetyloctopamine.

Animals↗
PubMed1982

Conjugated dopamine in superfusates of slices of rat striatum.

An acid-hydrolyzable conjugate of 3,4-dihydroxyphenylethylamine (dopamine, DA) was detected in superfusates from slices from rat striatum. The concentrations of endogenous free and conjugated DA, and of the acid metabolites (3,4-dihydroxyphenylacetic acid [DOPAC] and homovanillic acid [HVA]) in superfusates were measured using HPLC with electrochemical detection. Conjugated DA in superfusates represented 10-20% of the free DA under basal conditions and during release evoked by p-tyramine (5 X 10(-6) M to 5 X 10(-4) M); much smaller amounts of conjugated DA overflowed into superfusate when DA was released by equimolar concentrations of beta-phenylethylamine. Surprisingly, inhibition of monoamine oxidase by the inhibitors N-methyl-N-propargyl-3-(2,4-dichlorophenoxy)propylamine hydrochloride (clorgyline) or N-methyl-N-2-propynylbenylamine (pargyline) had little effect on the amounts of conjugated DA present in superfusate. Under basal conditions, the amounts of conjugated DA in superfusate were always less than the amounts of DOPAC but quite similar to the amounts of HVA. However, during release of DA evoked by p-tyramine the concentrations of conjugated DA in superfusate showed much more pronounced increases than those of the acidic metabolites.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Effects of aging on p- and m-octopamine, catecholamines, and their metabolizing enzymes in the rat.

Functions of octopamine in the mammalian brain are still not well known. An important aspect of this problem is the relationship between octopamines and catecholamines. Previous data have shown that their respective ontogenic evolutions are not parallel. Do the changes in brain related to aging also differentially affect these two groups of molecules? In order to check this point, the brain levels of p- and m-octopamine, p-tyramine, noradrenaline, and dopamine, as well as the activities of metabolizing enzymes, were determined in young adult and aging rats (20-26 months). Unlike catecholamines, there is a drastic decrease of p-octopamine after 20 months of age in the hypothalamus and telencephalon. p-Tyramine levels are also lowered. This change appears to be due to a decrease of the aromatic L-amino acid decarboxylase activity. These data, as those of ontogenic studies, confirm that p-octopamine and catecholamine metabolisms may have some independent steps and, moreover, that p-octopamine may have a role in the normal activity of the brain.

2-Hydroxyphenethylamine↗
PubMed1992

Determination of acidic metabolites of biogenic amines in human aqueous humour by gas chromatography--negative ion chemical ionisation mass spectrometry.

The concentrations of acidic metabolites derived from the biogenic amines o-, m-, and p-tyramines (o-, m-, and p-hydroxyphenylacetic acids), p-octopamine/p-synephrine (p-hydroxymandelic acid), and dopamine (homovanillic acid and 3,4-dihydroxyphenylacetic acid) were measured in human aqueous humour obtained from patients undergoing elective surgery for cataract removal or for trabeculectomy as a treatment for chronic open-angle glaucoma. There were no clear differences in the pattern of metabolism of neurotransmitters between the two groups. An unexpected finding was that the o-tyramine metabolite, o-hydroxyphenylacetic acid, was present in aqueous humour.

Acids↗
PubMed2004

Mammalian central nervous system trace amines. Pharmacologic amphetamines, physiologic neuromodulators.

The presence of the so-called trace amines 2-phenylethylamine, m-tyramine, p-tyramine, m-octopamine, p-octopamine and tryptamine in the mammalian central nervous system has been known for several decades. Despite much initial interest, these amines have largely been thought of as little more than metabolic by-products. The recent description of a family of mammalian trace amine receptors has, however, seen a resurgence of interest in the physiological role of this class of compounds. Although the trace amines are well documented to cause amphetamine-like effects, such responses only occur at concentrations multiple orders of magnitude above normal physiological levels. As such, it seems unlikely that these responses reflect the true physiological role of the trace amines. In this article previous studies showing responses to physiologically relevant concentrations of trace amines are reviewed, along with those showing a reciprocal relationship between trace amine levels and fluctuations in basal monoaminergic tone. On the basis of these studies it is hypothesized that the trace amines function as endogenous neuromodulators of classical monoamine neurotransmitters. These effects are seen as an altered neuronal sensitivity to monoamine neurotransmitters, with no change in neuronal excitability in the absence of neurotransmitter.

Amphetamines↗
PubMed2004

Inhibition of brain mitochondrial respiration by dopamine and its metabolites: implications for Parkinson's disease and catecholamine-associated diseases.

A structure-potency study examining the ability of dopamine (DA), its major metabolites and related amine and acetate congeners to inhibit NADH-linked mitochondrial O(2) consumption was carried out to elucidate mechanisms by which DA could induce mitochondrial dysfunction. In the amine studies, DA was the most potent inhibitor of respiration (IC(50) 7.0 mm) compared with 3-methoxytryramine (3-MT, IC(50) 19.6 mm), 3,4-dimethoxyphenylethylamine (IC(50) 28.6 mm), tyramine (IC(50) 40.3 mm) and phenylethylamine (IC(50) 58.7 mm). Addition of monoamine oxidase (MAO) inhibitors afforded nearly complete protection against inhibition by phenylethylamine, tyramine and 3,4-dimethoxyphenylethylamine, indicating that inhibition arose from MAO-mediated pathways. In contrast, the inhibitory effects of DA and 3-MT were only partially prevented by MAO blockade, suggesting that inhibition might also arise from two-electron catechol oxidation and quinone formation by DA and one-electron oxidation of the 4-hydroxyphenyl group of 3-MT. In the phenylacetate studies, 3,4-dihydroxyphenylacetic acid (DOPAC) was equipotent with DA in inhibiting respiration (IC(50) 7.4 mm), further implicating the catechol reaction as the cause of inhibition. All other carboxylate congeners; phenylacetic acid (IC(50) 13.0 mm), 4-hydroxyphenylacetic acid (IC(50) 12.1 mm), 4-hydroxy-3-methoxyphenylacetic acid (HVA, IC(50) 12.0 mm) and 3,4-dimethoxyphenylacetic acid (IC(50) 10.2 mm), were equipotent respiratory inhibitors and two- to fourfold more potent than their corresponding amine. These latter findings suggest that the phenylacetate ion can also contribute independently to mitochondrial inhibition. In summary, mitochondrial respiration can be inhibited by DA and its metabolites by four distinct MAO-dependent and independent mechanisms.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1958

Sensitization of the heart and nictitating membrane of the cat to sympathomimetic amines by antihistamine drugs.

Sensitization to the cardio-accelerator action of adrenaline and noradrenaline by five antihistamines was examined on the acutely denervated heart of the cat. Antazoline (Antistin), chlorcyclizine and promethazine (Phenergan) increased the cardio-accelerator responses to both amines equally. Mepyramine (Anthisan) increased noradrenaline more than adrenaline action. Diphenhydramine (Benadryl) resembled cocaine in potentiating the responses to noradrenaline but not to adrenaline.On the nictitating membrane mepyramine caused sensitization to the actions of adrenaline, noradrenaline and tyramine, an effect similar to that of chronic preganglionic denervation. Diphenhydramine enhanced the action of noradrenaline more than that of adrenaline and had little effect on tyramine action, giving a sensitization which bears a greater resemblance to the type caused by cocaine or chronic postganglionic denervation.It is suggested that two distinct mechanisms are required to account for the phenomena of sensitization.

Amines↗
PubMed1959

A hypothesis concerning the effect of cocaine on the action of sympathomimetic amines.

There is a store, perhaps in chromaffin tissue, of noradrenaline in tissues with a sympathetic innervation. The store is depleted by treatment with reserpine. Sympathomimetic amines like tyramine act only when this store is present and have no effect when the store is depleted. They also fail to act in the presence of cocaine. Catecholamines like noradrenaline have a much greater action than usual when the store is depleted, and they have a much greater action in the presence of cocaine. It is suggested that cocaine has the effect of blocking release from the store, so that the action of tyramine is abolished and the spontaneous release from the store which is responsible for the normal (low) sensitivity to noradrenaline is stopped. Noradrenaline is taken up into the store in the heart and the vessel wall from the blood, and the disappearance of noradrenaline from the blood is in part due to this uptake and not entirely to destruction. Cocaine may prevent this uptake of noradrenaline by the tissue stores. Experiments on rabbit atria, on the vessels of the rabbit ear and on the heart-lung preparation are described which are consistent with this hypothesis.

Animals↗
PubMed1960

The action of sympathetic blocking agents on isolated and innervated atria and vessels.

A preparation is described of isolated rabbit atria with both vagus and sympathetic nerves. The action on it of bretylium and of choline 2,6-xylyl ether bromide (TM10) was studied. A concentration of breylium sufficient to abolish the response to sympathetic stimulation also depressed the response to vagal stimulation. The effect was reversible, though more easily with choline xylyl ether. Both drugs abolished the accelerating action of acetylcholine in the presence of atropine, but they augmented the action of tyramine, and did not reduce that of amphetamine. In the vessels of the perfused rabbit ear they abolished the constrictor effect of nervous stimulation and of acetylcholine, but increased that of tyramine.

Acetylcholine↗
PubMed1960

Effect of denervation and of cocaine on the action of sympathomimetic amines.

The secretory effect of sympathomimetic amines on the submaxillary gland of cats was increased after section of the chorda tympani (preganglionic, parasympathetic supply). After sympathetic denervation of the gland the secretory response to tyramine and phenylethylamine was absent, the response to dopamine and ephedrine decreased and the response to adrenaline and noradrenaline increased. Large doses of cocaine, given locally into the gland, produced changes similar to those observed after sympathetic denervation. The sensitization towards adrenaline and noradrenaline was obtained with smaller doses. Tyramine did not cause a release of catechols from the suprarenal glands of the cat.

Animals↗
PubMed1961

Uptake of labelled noradrenaline by isolated atria.

The uptake of labelled noradrenaline by isolated rabbit atria has been studied, and the rate of outflow of radioactivity after a period of loading has been recorded. There is first a rapid outflow presumably from extracellular space, followed by a slow outflow presumably from intracellular space. Cocaine greatly diminished the intracellular uptake. Tyramine caused an increased outflow of radioactivity from intracellular sites which was not due to the increase in atrial rate, since noradrenaline which increased the rate more than tyramine had less effect on the outflow.

Animals↗
PubMed1962

Mechanism of cardiovascular actions of heptanolamines.

It has been suggested that heptaminol and methylheptaminol should be used as myocardial stimulants because they have cardiotonic actions similar to those of cardiac glycosides. However, as these aliphatic amines show definite sympathomimetic effects, the mechanism of their actions on the heart was investigated, in order to determine whether digitalis-like properties are involved in these effects. The pattern of pharmacological actions of heptaminol and methylheptaminol was compared with that of catechol amines, tyramine and k-strophanthin. The influence of atropine, hexamethonium, cocaine and reserpine was also investigated. The results show that both heptanolamines have a long-lasting cardiostimulant action which is abolished by cocaine and absent in reserpine pretreated animals. The pharmacological activity of these drugs may be entirely attributed to an indirect sympathomimetic action of the tyramine type, probably due to release of endogenous catechol amines. None of the experimental findings is consistent with the alleged digitalis-like action of these compounds.

Amines↗
PubMed1962

Relation in rat hind-limb blood vessels between nervous vasomotor tone and the response to vasoconstrictor drugs.

When the nervous component of the vasomotor tone of the blood vessels of the innervated rat hind limb perfused with blood was reduced by ganglion blockade, by section of the nerves to the hind limb, or by the indirect effect of drugs, the vasoconstrictor response of the blood vessels to noradrenaline was immediately increased. This increased peripheral response was observed only when the blood perfusing the hind limb was from the same animal or from a genetically similar animal. Reduction of the nervous component of the vasomotor tone also increased the constrictor response of the hind-limb blood vessels to adrenaline, ephedrine, tyramine and 5-hydroxytryptamine, but did not increase the response to angiotensin, vasopressin or S-methyl isothiourea. Pre-treatment with reserpine increased the hind-limb response to noradrenaline but reduced the response to ephedrine, tyramine and 5-hydroxytryptamine. The results suggest that, in rats, activity in the sympathetic nervous system directly influences the reactivity of peripheral blood vessels to noradrenaline and other sympathomimetic drugs.

Animals↗
PubMed1962

Some cocaine-like actions of 3-phenoxypro-pylguanidine.

In anaesthetized cats 3-phenoxypropylguanidine caused a contracture of the nictitating membrane, a dilatation of the pupil and a fall followed by a rise in the arterial blood pressure. In spinal preparations of cats the initial fall in blood pressure was usually absent and the rise in blood pressure subsided to a steady level, which was about 10 mm Hg above the initial pressure. The pressor action and the contracture of the nictitating membrane were inhibited by phenoxybenzamine and by previous treatment with reserpine, but were not abolished by adrenalectomy and bretylium. 3-Phenoxypropylguanidine potentiated the actions of adrenaline and noradrenaline, increased the blood glucose concentration of the rabbit and decreased the appetite of the cat. The action of tyramine on the cardiovascular system was inhibited by 3-phenoxypropylguanidine, but the stimulant action of tyramine on the nictitating membrane of the cat was not abolished by this substance. Although 3-phenoxypropylguanidine produced a local anaesthesia of long duration in guinea-pig skin, it failed to anaesthetize the rabbit cornea. The responses to stimulation of the preganglionic cervical sympathetic nerve of the cat and the great auricular nerve of the rabbit ear were not abolished by 3-phenoxypropylguanidine; neither did this substance abolish the nicotinic action of acetylcholine in atropinized cats. Contractions of the rat fundus to tryptamine and 5-hydroxytryptamine were antagonized by 3-phenoxypropylguanidine, but were potentiated by cocaine.

Acetylcholine↗
PubMed1962

Comparison of bretylium and guanethidine: tolerance, and effects on adrenergic nerve function and responses to sympathomimetic amines.

Bretylium depresses the slope of regression lines relating frequency of sympathetic nerve stimulation to magnitude of contractions of the cat nictitating membrane. In contrast, guanethidine and reserpine preferentially abolish responses to low rates of nerve stimulation and cause a roughly parallel shift of the regression lines. The hypersensitivity of the nictitating membranes of cats to intravenous adrenaline or noradrenaline is far greater after a series of small daily doses of bretylium or guanethidine than after single large doses. The maximal sensitivity produced was similar to that after postganglionic sympathetic nerve section and exceeded that produced by ganglion blockade. The development of hypersensitivity to catechol amines is accompanied by some return of responses of the nictitating membranes to sympathetic nerve stimulation despite continued daily administration of bretylium or guanethidine. In cats given bretylium daily, responses to low rates of nerve stimulation become greater than in controls unless the dose of bretylium given subcutaneously is 50 mg/kg or more. When marked hypersensitivity to catechol amines has been produced by giving bretylium or guanethidine daily for 7 or 14 days, the sympathomimetic effects of these compounds are greater. Responses to intravenous dimethylphenylpiperazinium are also increased and the results suggest that even large daily doses of adrenergic neurone blocking agents do not appreciably impair the functioning of the adrenal medulla. The pressor effects of intravenous adrenaline, noradrenaline and dimethylphenylpiperazinium iodide increase less than the corresponding nictitating membrane responses. These results are discussed in relation to tolerance to adrenergic neurone blockade, and differences between the effects of bretylium and guanethidine found in man. Bretylium and guanethidine depress the slopes of the dose-response curves for the pressor and nictitating membrane contracting effects of tyramine. When single doses or a short series of daily doses were given, guanethidine caused more depression of the slopes than did bretylium, but nevertheless large depressions of slope were found after giving bretylium daily for several weeks. The magnitude of the responses can be greater or less than in controls depending on the dose of the sympathomimetic amine, the dose of the adrenergic neurone blocking agent and the duration of its administration. The results suggest that injection of tyramine produces a progressively smaller release of adrenaline or noradrenaline during the daily administration of bretylium (or guanethidine) but that in some test situations this is more than compensated for by the development of hypersensitivity to the catechol amine released. Some corresponding changes in responses to amphetamine and ephedrine are also described.

Adrenergic Agents↗
PubMed1968

The effects of some beta-adrenoreceptor blocking drugs on the uptake and release of noradrenaline by the heart.

1. The potencies of some beta-adrenoreceptor blocking drugs in reducing noradrenaline uptake by the isolated heart were compared with their potencies in reducing the release of noradrenaline from the heart by tyramine.2. Of the drugs tested, propranolol, pronethalol and dichloroisoprenaline were the most potent in blocking uptake and release of noradrenaline, although none was at potent as cocaine; MJ 1999 and I.C.I. 50172 were only weakly effective.3. Pronethalol and dichloroisoprenaline each reduced release of noradrenaline by tyramine in the concentration range (10(-7)-10(-6)M) where blockade of responses to tyramine was apparent; with these drugs both reduction of noradrenaline release and beta-receptor blockade contribute to the reduction in responses to tyramine.4. Potency of beta-receptor blocking drugs in reducing noradrenaline uptake is unrelated to potency in blocking beta-receptors; Kö 592 blocks beta-receptors without affecting noradrenaline uptake.

Anilides↗
PubMed1969

Modification of the vasoconstrictor action of sympathomimetic agents by bretylium tosylate and tranylcypromine in man.

1. The vasoconstrictor actions of tyramine, methylamphetamine and ephedrine on the blood vessels of the human hand have been found to be potentiated by administration intra-arterially of the adrenergic neurone blocking agent, bretylium tosylate.2. One mechanism suggested for the enhancement of vasoconstriction is that bretylium possesses monoamine oxidase inhibiting activity, which, in the case of tyramine, is protective both to the sympathomimetic agent and the intra-neuronal transmitter which it releases. In the case of methylamphetamine and ephedrine, which are not substrates for the enzyme, protection of the intra-neuronal transmitter alone might occur, accounting for the lesser degree of potentiation of the effect of these amines by bretylium.3. Comparison of the influences of bretylium and the monoamine oxidase inhibitor, tranylcypromine, on the vasoconstrictor action of the sympathomimetic agents shows a similar pattern of enhancement in the presence of both these drugs.4. Tranylcypromine caused enhancement of the response of the hand vessels to noradrenaline, and this action could contribute to its potentiation of the effect of the sympathomimetic amines.5. For a monoamine oxidase inhibiting action of bretylium to be effective in potentiating the constrictor actions of the sympathomimetic agents on the hand blood vessels at a time when reflex sympathetic activity is blocked it is necessary to postulate that these drugs and reflex nerve activity act either on different compartments of the transmitter store or by different release mechanisms.

Bretylium Compounds↗