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PubMed1998

Differential trace amine alterations in individuals receiving acetylenic inhibitors of MAO-A (clorgyline) or MAO-B (selegiline and pargyline).

Marked, dose-dependent elevations in the urinary excretion of phenylethylamine, para-tyramine, and meta-tyramine were observed in depressed patients treated for three or more weeks with 10, 30, or 60 mg/day of the partially-selective inhibitor of MAO-B, selegiline (l-deprenyl). In comparative studies with other, structurally similar acetylenic inhibitors of MAO, pargyline, an MAO-B > MAO-A inhibitor used in doses of 90 mg/day for three or more weeks, produced elevations in these trace amines which were similar to those found with the highest dose of selegiline studied. Clorgyline, a selective inhibitor of MAO-A used in doses of 30 mg/day for three or more weeks (a dose/time regimen previously reported to reduce urinary, plasma, and cerebrospinal fluid 3-methoxy-4-hydroxyphenylethyleneglycol (MHPG) > 80%, indicating a marked inhibitory effect on MAO-A in humans in vivo) produced negligible changes in trace amine excretion. In comparison to recent studies of individuals lacking the genes for MAO-A, MAO-B, or both MAO-A and MAO-B, the lack of change in trace amine excretion in individuals with a mutation affecting only MAO-A is in agreement with the observed lack of effect of clorgyline in the present study. Selegiline produced larger changes in trace amines--at least at the higher doses studied--than found in individuals lacking the gene for MAO-B, in agreement with other data suggesting a lesser selectivity for MAO-B inhibition when selegiline was given in doses higher than 10 mg/day. Overall, trace amine elevations in individuals receiving the highest dose of deprenyl or receiving pargyline were approximately three to five-fold lower than the elevations observed in individuals lacking the genes for both MAO-A and MAO-B, suggesting that these drug doses yield incomplete inhibition of MAO-A and MAO-B.

Biogenic Amines↗
PubMed1994

Some kinetic properties of guinea pig liver monoamine oxidase.

Titration of monoamine oxidase activity in isolated guinea pig liver mitochondria with clorgyline and assay of remaining activity with tyramine yielded biphasic inhibition curves. The position of the plateaus obtained with mitochondria from four animals, indicated that the B form of monoamine oxidase accounted for 30% to 70% of the tyramine deaminating activity. Benzylamine deamination was selectively inhibited by (-)-deprenyl. However, benzylamine and other amines which are selective substrates for the B form of monoamine oxidase from the rat, were deaminated at only low rates by the guinea pig liver enzyme. Guinea pig liver contains a monoamine oxidase-B which is unusual in that although it exhibits apparently normal sensitivity to selective irreversible inhibitors, it has a low catalytic activity with substrates which the enzyme from rat liver deaminates rapidly.

Animals↗
PubMed1996

Nonexocytotic noradrenaline release induced by pharmacological agents or anoxia in human cardiac tissue.

In acute myocardial ischemia, noradrenaline is released locally from sympathetic varicosities by a Ca(2+)-independent nonexocytotic release mechanism that is effectively suppressed by inhibitors of the neuronal noradrenaline carrier (uptake1). The purpose of the present study was to elucidate the significance of free axoplasmic amine concentration and disturbed neuronal sodium homeostasis for nonexocytotic noradrenaline release in the human heart by comparing the release induced by anoxia with that induced by reserpine, tyramine, or veratridine. The overflow of endogenous noradrenaline and dihydroxyphenylethyleneglycol was assessed in human atrial tissue incubated in calcium-free Krebs-Henseleit-solution to prevent interferences by exocytotic release. The overflow of dihydroxyphenylethyleneglycol served as indicator of the free axoplasmic noradrenaline concentration. When vesicular uptake was blocked by the reserpine-like agent Ro 4-1284, high dihydroxyphenylethyleneglycol overflow was observed without concomitant noradrenaline overflow. If, however, Ro 4-1284 was combined with sodium pump inhibition (by omission of extracellular potassium) or with alteration of the transmembrane sodium gradient (by lowering the extracellular sodium concentration), both dihydroxyphenylethyleneglycol and noradrenaline were released. The indirectly acting sympathomimetic tyramine induced a marked increase in noradrenaline overflow which was accompanied by overflow of high amounts of dihydroxyphenylethyleneglycol, indicating interference of the drug with both vesicular catecholamine transport and amine transport via uptake1. Likewise, veratridine induced an overflow of noradrenaline (which was prevented by blockade of uptake1) and dihydroxyphenylethyleneglycol indicating a reserpine-like action of the drug. A disturbed energy status of the sympathetic neuron induced by cyanide intoxication or anoxia caused noradrenaline overflow which was suppressed by uptake1 blockade. Blockade of sodium channels by tetrodotoxin effectively reduced noradrenaline overflow during cyanide intoxication but not during anoxia. Anoxia-induced noradrenaline release, however, was markedly suppressed by inhibition of Na+/H+ exchange with ethylisopropylamiloride, indicating the Na+/H+ exchange as the predominant pathway for sodium entry into the sympathetic neuron during anoxia. The results demonstrate that disturbed neuronal sodium homoeostasis and impaired vesicular storage function are critical conditions, causing nonexocytotic noradrenaline release in anoxic human cardiac tissue.

Cell Membrane↗
PubMed1996

Selective enhancement by an adenosine A1 receptor agonist of agents inducing contraction of the rat vas deferens.

The adenosine analogue N6-cyclopentyladenosine (CPA), acting via postjunctional A1 receptors, has been shown to enhance contractions of the rat vas deferens induced by adenosine 5'-triphosphate (ATP), the sympathetic cotransmitter in this tissue. The aim of the present study was to examine the ability of CPA to enhance contractions induced by other contractile agents. CPA (0.01-0.3 microM) enhanced contractions induced by exogenous ATP (10 microM), 5-hydroxytryptamine (5-HT) (3 microM), tyramine (10 microM), 2-methyl-5-hydroxytryptamine (2-Me-5-HT) (10 microM) and KCl (35 mM) and this enhancement was blocked by an A1-selective concentration (3 nM) of 1, 3-dipropyl-8-cyclopentylxanthine (DPCPX). CPA failed to enhance contractions induced by exogenous noradrenaline (NA) (1 microM or 10 microM), bradykinin (0.1 microM), phenylephrine (3 microM) or carbachol (10 microM). The contractions induced by ATP (10 microM), 5-HT (3 microM), 2-Me-5-HT (10 microM) and KCl (35 mM) were unaffected by tetrodotoxin (1 microM) as well as by desensitisation of the P2x-purinoceptors with the ATP analogue adenosine 5'-(alpha, beta-methylene) triphosphonate. The contractions induced by tyramine (10 microM) and 2-Me-5-HT (10 microM) were blocked by prazosin (100 nM) or by imipramine (1 microM). Ketanserin (10 nM) antagonised the response to 5-HT giving a dose-ratio of 12.9 corresponding to an apparent pA2 of 9.1. In conclusion, the A1-mediated effect was clearly selective for certain contractile agents and not due to a non-specific increase in contractility of the tissue. CPA enhanced contractions induced by both ATP and indirect sympathomimetics which release endogenous NA, and this enhancement of the two sympathetic cotransmitters may have a functional significance, and demonstrates the complexity of the neuromodulatory effects of adenosine in the rat vas deferens.

Adenosine↗
PubMed1991

Carrier-mediated outward transport of dopamine from adrenergic varicosities of the vas deferens of reserpine-pretreated rats.

In vasa deferentia of reserpine-pretreated rats a carrier-mediated (i.e., desipramine-sensitive) outward transport of endogenous dopamine was induced by either tyramine or ouabain. The dopamine taking part in the efflux induced by tyramine (and the concomitant efflux of DOPAC) was derived from ongoing synthesis of dopamine. Inhibition of MAO trebled the rate of spontaneous efflux of dopamine and reduced the spontaneous efflux of DOPAC by 90%. After inhibition of MAO, desipramine caused a further five-fold increase in the basal efflux of dopamine with no change in the basal efflux of DOPAC. Inhibition of COMT failed to affect the spontaneous efflux of dopamine but increased that of DOPAC. It is concluded that, after depletion of the noradrenaline stores by pretreatment with reserpine, an outward transport of axoplasmic dopamine is induced by the same mechanisms that (without any pretreatment with reserpine) are known to initiate an outward transport of noradrenaline.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1991

Involvement of alpha 1- and alpha 2-adrenoceptors in the responses of proximal and distal segments of the canine saphenous vein to exogenous and endogenous noradrenaline.

In the present study the relationship between adrenergic nerve terminals and postjunctional alpha-adrenoceptors mediating the responses to the endogenous transmitter was compared at proximal and distal levels of the canine saphenous vein. Concentration-response curves to noradrenaline and to tyramine as well as frequency-response curves to electrical stimulation were compared at both levels of the vessel, in the absence and presence of either prazosin (100 nmol.l-1) or yohimbine (100 nmol.l-1). The influence of inhibition of neuronal uptake by cocaine (12 mumol.l-1) on the responses to noradrenaline in the presence of prazosin (56 nmol.l-1) or yohimbine (20 nmol.l-1) was compared at the proximal level. The results show that, at the proximal level, the maximal responses to electrical stimulation and tyramine reached 80.1 +/- 2.2 (n = 18) and 74.2 +/- 1.9 (n = 18)%, respectively, of the maximal responses to noradrenaline, and 70.3 +/- 0.8 (n = 15) and 53.1 +/- 1.2 (n = 14)%, respectively, at the distal level. Furthermore, the proximal strips were more sensitive to electrical stimulation than the distal ones. Prazosin had a much greater inhibitory effect on the contractile responses to noradrenaline than on those to electrical stimulation, at both levels. At proximal level, the shifts (to the right) of the concentration (frequency)-response curves (at EC50) amounted to 0.58 +/- 0.02 (n = 16) and 0.18 +/- 0.02 (n = 8) log units, respectively (P less than 0.05), but, at the distal level, to 1.12 +/- 0.03 (n = 16) and 0.28 +/- 0.08 (n = 8) log units, respectively (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Neuropeptide Y differentiates between exocytotic and nonexocytotic noradrenaline release in guinea-pig heart.

The overflow of neuropeptide Y (NPY; radioimmunoassay), noradrenaline and dihydroxyphenylethylenglycol (DOPEG; high pressure liquid chromatography) from guinea-pig perfused hearts was investigated in relationship to exocytotic and nonexocytotic release mechanisms. Exocytotic release: Electrical stimulation of the left stellate ganglion (12 Hz; 1 min) evoked a calcium-dependent overflow of noradrenaline and NPY, that was accompanied by a minor and prolonged increase in DOPEG overflow. This increase in DOPEG overflow was attenuated by blockade of neuronal amine re-uptake. In the presence of calcium, a closely related co-release of noradrenaline and NPY was also observed during administration of veratridine (10 microM); it was completely prevented by tetrodotoxin (1 microM). Nonexocytotic release: In the absence of extracellular calcium, veratridine (30 microM) induced noradrenaline overflow only when combined with the reserpine-like agent Ro 4-1284 (10 microM). This overflow was accompanied by efflux of DOPEG, but not of NPY. Similarily, tyramine (1-100 microM) induced a calcium-independent concomitant overflow of both noradrenaline and DOPEG, but not of NPY. During anoxic and glucose-free perfusion a predominantly calcium-independent overflow of noradrenaline was observed; only in the presence of extracellular calcium was this overflow accompanied by a minor overflow of NPY. Noradrenaline overflow, induced by veratridine plus Ro 4-1284 (in the absence of calcium), by tyramine, or by anoxia, was suppressed by blockade of neuronal amine re-uptake, and was, therefore, mediated by reversed transmembrane amine transport by the neuronal uptake carrier. The results indicate that NPY is co-released with noradrenaline only during calcium-dependent exocytosis.(ABSTRACT TRUNCATED AT 250 WORDS)

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1977

Purification and properties of human serum dopamine-beta-hydroxylase.

1. Two different molecular forms of dopamine-beta-hydroxylase were isolated from human serum; a major component (Peak I enzyme) with a molecular weight of 368000 and with a higher specific activity and a minor component (Peak II enzyme) with a molecular weight of 188000 and with a lower specific activity. 2. Both forms require ascorbic acid for the activity, and are stimulated by fumarate. Addition of N-ethylmaleimide or copper also increased the activity. The optimal pH of both forms in the presence of 20mM tyramine as substrate is 5.0. 3. Km values toward tyramine of Peak I enzyme and Peak II enzyme were 1.67 mM and 14.2 mM respectively. 4. Both Peak I enzyme and Peak II enzyme are glycoprotein.

Animals↗
PubMed1992

The effects of sympathetic nervous system activation and psychological stress on glucose metabolism and blood pressure in subjects with type 2 (non-insulin-dependent) diabetes mellitus.

The sympathetic nervous system may contribute to excessive hepatic glucose output in Type 2 (non-insulin dependent) diabetes mellitus and could be implicated in the interrelated problem of hypertension. The aim of these studies was to determine whether subjects with Type 2 diabetes had normal sensitivity (compared with age- and weight-matched non-diabetic subjects) to noradrenaline infusion (60 ng.kg-1.min-1 for 60 min) and to compare the responses with oral tyramine administration (800 mg), and psychological stress (using competitive computer games). Noradrenaline infusion caused significantly greater plasma glucose (mean increment 2.1 +/- 0.4 vs 0.6 +/- 0.1 mmol/l, p less than 0.005) and pressor responses (mean systolic increment 21 +/- 3 vs 11 +/- 1 mmHg, p less than 0.02) in the diabetic subjects. The excessive glycaemia was due to increased hepatic glucose output rather than reduced glucose disposal. Tyramine administration caused significantly increased hepatic glucose output and plasma glucose levels, but with similar responses in the diabetic and non-diabetic subjects; the pulse and pressor responses were also similar between the groups. The psychological stressor induced significant increases in pulse, blood pressure and non-esterified fatty acid levels in the combined group of subjects (p less than 0.01) but did not influence plasma glucose levels in either diabetic or non-diabetic subjects. We conclude that pharmacologically-induced sympathetic nervous stimulation can induce hyperglycaemia. Subjects with uncomplicated Type 2 diabetes have increased sensitivity to exogenous noradrenaline but may not hyperrespond to endogenous sympathetic activation.

Blood Glucose↗
PubMed1979

Morphine abstinence and serotonin supersensitivity in man: analogies with the mechanism of migraine?

Supersensitivity to serotonin during migraine attack has been previously observed. Since the attack has been attributed to a critical lowering of morphine-like factors, we can expect serotonin supersensitivity during morphine abstinence. Slight signs of morphine abstinence have also been induced in volunteers after mild (10-24 mg/day) and limited (3 days) treatment. To evaluate the sensitivity to serotonin, dopamine, noradrenaline, and tyramine in the smooth muscle of the hand dorsal vein, in vivo, the computerized venotest was applied before, during, and 24 h after withdrawal of morphine. Venous sensitivity to serotonin and dopamine (but not to noradrenaline and tyramine) increased 10- to 20-fold after morphine withdrawal. Venous monoamine supersensitivity in morphine abstinence, similar to that observed during migraine attacks, could be indirect evidence of an analogous mechanism in both conditions.

Adult↗
PubMed1980

Inotropic effect of prostacyclin (PGI2) on isolated rat atria at different contraction frequencies.

The effects of a wide range of Prostacyclin (PGI2) concentrations on the Isometric Developed Tension (IDT) of isolated left auricles driven at different frequencies (0.8, 1.6 or 3.3 Hz) were explored. A comparison of the positive inotropism of PGI2, norepinephrine (NE), tyramine and phenylephrine (Phenyl) indicated that PGI2, NE and tyramine enhanced peak tension significantly less at slow (0.8 and 1.6 Hz) than at higher rates (3.3 Hz); whereas Phenyl augmented equally the IDT at all of these three driving frequencies. The positive inotropism evoked by PGI2 was inhibited by (-)-propranolol and also by a treatment with 6-OHDA. Cocaine, normetanephrine and U-0521, augmented the positive inotropic influence of PGI2 on atria paced at a slow rate (0.8 Hz) but not at a faster one (3.3 Hz). These results suggest that the action of PGI2 on atrial contractions is apparently indirect and mediated by the release of tissue catecholamines. In addition the effect of PGI2 and NE at slow and fast rates appears associated with a different relative relevance of the processes which terminate the action of added sympathomimetic agonists, namely, neuronal or extraneuronal uptake as well as metabolization via COMT. These mechanisms seen to be more prominent at slower driving frequencies and could explain the diminished effect of PGI2 and NE on slowly paced atria.

Animals↗
PubMed1985

Phorbol ester, an activator of protein kinase C, enhances calcium-dependent release of sympathetic neurotransmitter.

The effect of phorbol ester, phorbol 12,13-dibutyrate, was investigated on the overflow of tritium from 3H-noradrenaline-loaded sympathetic neurons of the isolated perfused salivary gland of the rat. Stimulation (1 Hz for 60 s)-evoked overflow of tritium was enhanced by phorbol ester. A significant enhancement was seen at 1 nmol/l, which increased to a maximum level (over 4-fold) at 30 nmol/l. The spontaneous overflow of radioactivity, however, was not affected by any concentration of phorbol ester. The facilitatory effect of phorbol ester on stimulation-evoked overflow was observed in the presence of inhibitors of neuronal and extraneuronal uptake as well as after removal of negative feedback inhibition of release by presynaptic alpha-adrenoceptors. Tyramine (7 mumol/l for 10 min) caused a marked increase in the overflow of tritium in either the presence or absence of calcium. However, tyramine-induced overflow was not enhanced by phorbol ester. It is concluded that protein kinase C of sympathetic neurons is involved in an exocytotic release of the transmitter.

Animals↗
PubMed1982

Metabolism of endogenous and exogenous noradrenaline in the rabbit perfused heart.

The outflow of noradrenaline, 3,4-dihydroxyphenylglycol (DOPEG) and 3,4-dihydroxymandelic acid (DOMA) from rabbit perfused hearts was studied by chromatography on alumina followed by high pressure liquid chromatography with electrochemical detection. In the absence of drugs and without nerve stimulation, the outflow of endogenous noradrenaline over a period of 108 min averaged 0.17 pmol X g-1 X min-1 and the outflow of DOPEG 2.1 pmol X g-1 X min-1. The outflow of DOMA was below the detection limit (less than 0.13 pmol X g-1 X min-1). The effect of perfusion with (-)-noradrenaline 0.1, or 10 mumol/l for 18 min was then investigated. As the concentration of nor-adrenaline increased so did the outflow of DOPEG. Moreover, DOMA was found in the venous effluent during and after perfusion with noradrenaline 1 or 10 mumol/l. The increase in the outflow of DOPEG and DOMA was almost abolished when cocaine 10 mumol/l was present during the perfusion with noradrenaline 1 mumol/l. The release of endogenous noradrenaline by sympathetic nerve stimulation or tyramine 10 mumol/l, but not the release evoked by nicotine 30 mumol/l, was accompanied by an increase in the outflow of DOPEG; an outflow of DOMA was not observed. It is concluded that, in the rabbit perfused heart, DOPEG is an important metabolite of endogenous noradrenaline. DOMA is at best a minor product, either when the neurones are at rest or when noradrenaline is released by sympathetic nerve stimulation, nicotine or tyramine. DOMA is formed in detectable amounts when the tissue is exposed to a high concentration of exogenous noradrenaline. Like DOPEG, it is formed intraneuronally. The results confirm and extend those obtained previously on guinea-pig incubated atria. They make it unlikely that, in these tissues at least, DOMA formation is one of the physiological pathways of noradrenaline catabolism.

Animals↗
PubMed1976

The effects of methacholine and calcium deprivation on the release of the false transmitter, alpha-methyladrenaline, from the isolated rabbit heart.

1. Anaesthetized rabbits were infused for 20 min with 85 mug-kg-1-min-1(+/-)-alpha-methyladrenaline. The hearts dissected 15 min after the infusion contained 1.49 mug/g alpha-methyladrenaline; the endogenous noradrenaline content was correspondingly decreased. 2. Hearts from alpha-methyladrenaline-infused animals were isolated with the right sympathetic nerves intact and perfused. Ventricular rate, right atrial and right ventricular tensions were recorded using the transverse method. 3. Electrical stimulation (10 Hz, 1 ms, 1 min) of sympathetic nerves, perfusion with the nicotinic drug, p-aminophenethyltrimethylammonium (PAPETA) or perfusion with 54 mM KCl (high K+) solution evoked an output of both alpha-methyladrenaline and noradrenaline. The ratio of the amines in the perfusates was similar to that found in the hearts after termination of the experiments or in non-perfused hearts. 4. Methacholine perfused before and during sympathetic nerve stimulation, PAPETA or high K+ inhibited the release of both false transmitter and noradrenaline. These effects were reversed by atropine. Similarly, lowering the calcium chloride concentration of the medium from 1.8 to 0.1 mM decreased amine outputs. This was reversed by washing. 5. Tyramine evoked a preferential release of the false transmitter that was not altered by methacholine or calcium deprivation. 6. These experiments whow that the muscarinic inhibition of neuronal noradrenaline release and the requirement of calcium ions for its liberation by depolarizing stimuli can be extended to a false transmitter amine. It is suggested that the proportion of alpha-methyladrenaline to noradrenaline occurring in the perfusate during administration of tyramine reflects the relative concentrations of the amines in the axoplasm.

Aniline Compounds↗
PubMed1986

The role of co-transported sodium in the effect of indirectly acting sympathomimetic amines.

The adrenergic nerve endings of vasa deferentia of either untreated or reserpine (R) and/or pargyline (P) pretreated rats were loaded with 3H-noradrenaline; COMT was inhibited by U-0521 (U). After 100 min of wash-out with Ca2+-free solution, the efflux of tritium (and of 3H-noradrenaline) from the tissue was largely of neuronal origin and remained constant with time (when expressed as fractional rate of loss; FRL). After 110 min of wash-out the effect of inhibition of the Na+,K+-ATPase (by low K+ or ouabain) on basal and on sympathomimetic amine-induced efflux of tritium (or 3H-noradrenaline, under the condition U) was studied in paired experiments. Inhibition of the Na+,K+-ATPase caused a time-dependent increase in the efflux of tritium (or 3H-noradrenaline) which was inhibited by desipramine. Inhibition of the Na+,K+-ATPase also caused a time-dependent reduction of the initial rate of neuronal uptake of 3H-noradrenaline. The effectiveness of the sympathomimetic amines tyramine and amphetamine in inducing "release" (i.e., outward-transport) of noradrenaline depended on the experimental condition: it was most pronounced under the condition RPU, followed by the condition PU and lowest under the condition U (i.e., in tissue of untreated rats). Inhibition of the Na+,K+-ATPase caused an early and transient enhancement of the "release" of noradrenaline induced by tyramine or amphetamine. This enhancement was seen already within the first min after inhibition of the ATPase, i.e., before a pronounced inhibition of uptake (of noradrenaline) and before a pronounced increase of the basal efflux was observed.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphetamine↗
PubMed1982

Monoamine oxidase inhibition by tranylcypromine: assessment in human volunteers.

The inhibition of monoamine oxidase (MAO) by tranylcypromine was studied in 6 healthy volunteers given increasing doses of 10, 15, 20 and 25 mg/day over a 4-week period. Measurements were made of urinary tryptamine excretion, blood pressure response to tyramine (TY) and norepinephrine (NE), and subjective self-rating. A significant increase in urinary tryptamine, indicating the onset of MAO inhibition, occurred in all 6 subjects once the cumulative dose of 40 mg TC had been administered. Thereafter, urinary tryptamine increased up to 7-fold, dose-dependently with large interindividual variation (78 +/- 27 to 549 +/- 252 microgram/g creatinine). Within 4 days after stopping the drug, control values were reached again. The assessment of TY potentiation by comparison of equieffective doses (S dose) became up to 10 times more sensitive when both the height and the duration of the increase in systolic blood pressure (S AUC) were taken into account. The increases in tyramine sensitivity found with the highest cumulative doses of TC (5.4 +/- 0.8 mg/kg; n =6) were S dose from 8-16 and S AUC from 28-162, respectively. The pharmacodynamic half-life (Pd 1/2) of TC approximated a mean first fast Pd 1/2 of 1.3 d and a slower phase of 14.2 d. During treatment with the highest TC dose, resting blood pressure was significantly elevated from 120 to 128 mm Hg, and the pressor sensitivity to NE (S NE) in 4 of the 6 subjects rose, the mean was 1.7 (n = 6). In 3 volunteers NE sensitivity was normalized within 4 days after stopping TC. There was a significant correlation between increasing vigilance with TC dose in 5 volunteers (r = 0.81, n = 15, p less than 0.01). It is concluded that combination of the results of several tests has provided reliable information about the onset, extent and duration of MAO inhibition in healthy volunteers.

Adult↗
PubMed1976

Release of noradrenaline proposed as a mechanisms for the positive inotropic action of dipyridamole.

In the arterially blood-perfused canine papillary muscle, i.a. injections of dipyridamole (10-300 mug) produced a dose-dependent increase in developed tension amounting to about 45% of the basal developed tension at 300 mug. The positive inotropic response to dipyridamole was greatly reduced by a prior i.a. injection of propranolol (10 mug) or by pretreatment with reserpine (0.2 mg/kg s.c. for 3 consecutive days) but not affected by a prior i.a. injection of tetrodotoxin (1 mug) or desmethylimipramine (3-10 mug). The positive inotropic response to dipyridamole reduced by pretreatment with reserpine was restored by i.a. infusion of noradrenaline (0.03 mug/min). Dipyridamole did not modify the positive inotropic responses to noradrenaline and tyramine. These results suggest that the positive inotropic response to dipyridamole is largely due to noradrenaline released from adrenergic nerve endings by a mechanism that differs from those operative in the action of tyramine or in liberation of noradrenaline upon excitation.

Animals↗
PubMed1993

Analysis of biogenic amines in plasma of hypertensive patients and a control group.

Procedures were developed for the determination of 17 circulating amines using gas chromatography-negative ion chemical ionisation mass spectrometry. The amines were quantified against their appropriate deuterated isotopomers. The mean concentrations and ranges of catecholamines and trace amines were high compared with previous studies. In comparison with nonhypertensives, plasma from hypertensives had higher concentrations of the following amines: noradrenaline (t = 4.0%); normetanephrine (t = 6.1%) and metanephrine (t = 1.9%). There were no significant differences between 5HT levels in plasma from hypertensives and controls. The following trace amines could be detected in variable amounts in plasma: p-tyramine, m-tyramine, p-octopamine, m-octopamine, p-synephrine, m-synephrine, and salsolinol. The trace amines melatonin, N-acetyl 5HT, tryptamine, 6-hydroxymelatonin and 5-methoxytryptamine could not be detected in plasma with limits of detection lying in the range 20-100 pg ml-1.

Biogenic Amines↗