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PubMed2003

Failure of systemic hypoxia to blunt alpha-adrenergic vasoconstriction in the human forearm.

Systemic hypoxia in humans evokes forearm vasodilatation despite significant reflex increases in sympathetic vasoconstrictor nerve activity and noradrenaline spillover. We sought to determine whether post-junctional alpha-adrenergic vasoconstrictor responsiveness to endogenous noradrenaline release is blunted during systemic hypoxia. To do so, we conducted a two-part study in healthy young adults. In protocol 1, we measured forearm blood flow (FBF; venous occlusion plethysmography) and calculated the vascular conductance (FVC) responses to brachial artery infusions of two doses of tyramine (evokes endogenous noradrenaline release) in 10 adults during normoxia and mild systemic hypoxia (85 % O2 saturation; pulse oximetry of the earlobe). Systemic hypoxia evoked significant forearm vasodilatation as indicated by the increases in FBF and FVC (approximately 20-23 %; P < 0.05). The low and high doses of tyramine evoked significant reductions in FVC (vasoconstriction) that were similar in magnitude during normoxia (-29 +/- 3 and -53 +/- 4 %) and mild hypoxia (-35 +/- 4 and -58 +/- 3 %; P = 0.33). In protocol 2, forearm vasoconstrictor responses to the high dose of tyramine were determined in eight young adults during normoxia and during graded levels of systemic hypoxia (85, 80 and 75 % O2 saturation). The reductions in FVC were similar during normoxia (-59 +/- 2 %) and the three levels of hypoxia (85 % O2 saturation, -64 +/- 3 %; 80 % O2 saturation, -62 +/- 1 %; 75 % O2 saturation, -61 +/- 3 %; P = 0.37). In both protocols, the tyramine-induced increases in deep venous noradrenaline concentrations were similar during normoxia and all levels of hypoxia. Our results demonstrate that post-junctional alpha-adrenergic receptor vasoconstrictor responsiveness to endogenous noradrenaline release is not blunted during mild-to-moderate systemic hypoxia in healthy humans.

Adult↗

PubMed2005

Impaired modulation of sympathetic alpha-adrenergic vasoconstriction in contracting forearm muscle of ageing men.

Recent evidence indicates that older healthy humans demonstrate greater vasoconstrictor tone in their active muscles during exercise compared with young adults. Therefore, we tested the hypothesis that the normal ability of muscle contractions to blunt sympathetic alpha-adrenergic vasoconstriction (functional sympatholysis) is impaired with age in healthy humans. We measured forearm blood flow (FBF; Doppler ultrasound) and calculated the forearm vascular conductance (FVC) responses to alpha-adrenergic receptor stimulation during rhythmic handgrip exercise (15% maximum voluntary contraction) and during a control non-exercise vasodilator condition (intra-arterial adenosine infusion) in seven young (25 +/- 2 years) and eight healthy older men (65 +/- 2 year). FVC responses to intra-arterial tyramine (evokes endogenous noradrenaline release), phenylephrine (alpha1-agonist) and clonidine (alpha2-agonist) were assessed. In young men, the vasoconstrictor responses to tyramine (-25 +/- 1 versus -56 +/- 6%), phenylephrine (-11 +/- 4 versus -39 +/- 4%) and clonidine (-12 +/- 4 versus -38 +/- 5%; all P < 0.005) were blunted during exercise compared with adenosine. In contrast, exercise did not significantly blunt the response to tyramine (-30 +/- 2 versus -36 +/- 7%; P = 0.4) or phenylephrine (-16 +/- 2 versus -19 +/- 3%; P = 0.3) in older men, but did attenuate the response to clonidine (-22 +/- 3 versus -37 +/- 6%; P < 0.05). The magnitude of functional sympatholysis, calculated as the difference in the vasoconstrictor responses during adenosine infusion and exercise, was significantly lower in older compared with young men in the presence of tyramine (-6 +/- 7 versus -31 +/- 6%), phenylephrine (-3 +/- 3 versus -28 +/- 4%) and clonidine (-15 +/- 4 versus -26 +/- 3%; all P < 0.05). We conclude that ageing is associated with impaired functional sympatholysis in the vascular beds of contracting forearm muscle in healthy men. These findings might help explain the greater skeletal muscle vasoconstrictor tone and reduced blood flow during large muscle dynamic exercise in older adults.

Adenosine↗

PubMed1986

Studies of the free faecal amines of infants with gastroenteritis and of healthy infants.

The free primary amines present in the faeces of 44 infants (1-18 months) with gastroenteritis have been examined by field desorption mass spectrometry of the lactone form of their fluorescamine derivatives without their prior separation. p-Tyramine, 2-phenylethylamine, the diamines, putrescine and cadaverine and several of their acyl derivatives were common constituents, but a number of other amines were also characterised. Using thin layer chromatography and field desorption mass spectrometry of the amine dansyl derivatives a comparative study was made of the faecal amines of 13 selected infants with gastroenteritis (diarrhoea) and of 13 healthy infants. p-Tyramine, the most abundant amine, was significantly higher (p = 0.02) in the sick infants. The overall presence of p-tyramine was more significantly related to the diet of the infants. Faecal tyramine was low in breast fed infants but significantly higher (p = 0.01) in infants fed cow's milk.

Amines↗

PubMed1981

Cardiac catecholamine stores after cardiac sympathectomy, 6-OHDA, and cardiac denervation.

Sympathetic nerves are known to reach the heart via classical vagal pathways. Bilateral cervicothoracic sympathectomy (CS) might be expected therefore to leave significant amounts of releasable catecholamines in the myocardium if the vagi are left intact. Cardiac responses to tyramine (500 micrograms intracoronary) were compared in animals with CS, extrinsic cardiac denervation (CD), and chemical sympathectomy with 6-hydroxydopamine (6-OHDA). Dogs were placed on cardiopulmonary bypass and isovolumic pressures were recorded from the heart. In control animals, tyramine caused profound increases in rate (58%) and isovolumic pressures (86-170%). Ten CS animals demonstrated responses indistinguishable from control animals. Four CD and four 6-OHDA animals showed no response to tyramine. Cervical vagal stimulation after atropine in the CS animals produced tachycardia. Histofluorescent studies demonstrated the presence of significant numbers of cardiac adrenergic fibers in this group. The normal tyramine responsiveness of the CS animals was attributed to 1) significant numbers of vagal adrenergic fibers remaining in the heart after cervicothoracic sympathectomy, and 2) denervation supersensitivity, rendering the heart very responsive to the catecholamine that remains.

Animals↗

PubMed1975

Nonshivering thermogenesis and cold resistance in rats under severe cold conditions.

Following either chronic exposure to 6 degrees C, or outdoor winter exposure, or chronic treatment with tyramine rats were exposed to -40 degrees C and their oxygen consumption and colonic temperature monitored. Fall in body temperature with time of exposure followed a sigmoid curve which had an inflection point around 32.9 degrees C. Both the time required for body temperature to reach this point and hypothermic resistance defined as the total O2 consumed up to the inflection time were useful indices of resistance to severe cold; Three days before the cold tests, capacity for norepinephrine-induced nonshivering thermogenesis was measured in all animals by examination of their metabolic response to tyraminemthe magnitude of response to tyramine correlated well with hypothermic resistance only for those rats chroncally treated with tyramine. It is concluded that it is impossible to predict with any reasonable degree of confidence the cold resistance of a rat from its tyramine response. In cold-acclimated rats, factors in addition to norepinephrine sensitivity are significantly involved in cold resistance and deserve further studies.

Acclimatization↗

PubMed1983

Prejunctional and postjunctional actions of endogenous norepinephrine at the sympathetic neuroeffector junction in canine coronary arteries.

The effects of endogenous and of exogenous norepinephrine were studied in isolated rings of canine left circumflex coronary artery and its first ventricular branch. Norepinephrine was released from adrenergic nerve endings by transmural electrical stimulation and by tyramine. In rings contracted with prostaglandin F2 alpha, transmural electrical stimulation resulted in frequency-dependent relaxations which were blocked by propranolol or tetrodotoxin; tyramine and exogenous norepinephrine caused concentration-dependent relaxations which were blocked by propranolol. The tyramine-induced relaxations also were inhibited by cocaine. The left circumflex artery was less sensitive than its branch to beta-adrenergic activation; this difference was significant even between rings of the two vessels immediately adjacent to the branching point and was abolished by phentolamine. In the presence of propranolol, transmural electrical stimulation, tyramine and phenylephrine, produced contractions of the left circumflex artery, but not the branch; these contractions were prevented by phentolamine. Phentolamine, but not prazosin, augmented the beta-adrenergic response of left circumflex artery to low frequency stimulation; in arteries preincubated with 3H-norepinephrine, this was accompanied by an increased overflow of tritiated neurotransmitter. The prejunctional effect of phentolamine was also evident in branch coronary arteries which exhibit no postjunctional alpha-adrenergic responses. With high frequency stimulation, both alpha-adrenergic antagonists equally augmented the relaxation of left circumflex artery; the efflux of tritiated norepinephrine was not different from untreated arteries. These experiments demonstrate, in isolated coronary arteries, that the primary adrenergic response to released endogenous norepinephrine is beta-adrenergic relaxation. The prejunctional effects of nonspecific alpha-adrenergic antagonists preclude their use in determining the importance of postjunctional coronary alpha-adrenergic receptor activation caused by sympathetic nerve stimulation.

Adrenergic alpha-Antagonists↗

PubMed1970

Autonomic reflexes and vascular reactivity in experimental scurvy in man.

Ascorbic acid is a required cofactor in the conversion of dopamine to norepinephrine in vitro, and the deficiency of this vitamin in guinea pigs is associated with degeneration of autonomic ganglion cells and with cardiac supersensitivity to norepinephrine. Because of these findings, we tested the hypothesis that ascorbic acid deficiency in man alters autonomic cardiovascular reflexes and vasomotor responses to adrenergic stimuli. We studied five normal volunteers who had been deprived of ascorbic acid for a period of 3 months; they had developed symptoms and signs of scurvy and their plasma levels of ascorbic acid averaged 0.178 +/-SE 0.07 mg/100 ml. We repeated the studies after giving the subjects vitamin C for a period of 4 months; they had become asymptomatic and their plasma ascorbic acid had increased to an average of 1.68 +/-0.151 mg/100 ml. Blood flow to the left forearm (plethysmograph), arterial and central venous pressures, and heart rate were measured before and after exposure of the lower half of the body to subatmospheric levels of pressure and before and after intravenous and intra-arterial (left brachial artery) infusions of norepinephrine and tyramine. Average values of blood flow (7.9 +/-1.4 ml/min per 100 ml), arterial pressure (91.2 +/-4.6 mm Hg), heart rate (68 +/-4.4 beats/min), central venous pressure (6.1 +/-1.1 mm Hg), and plasma catecholamines (0.68 +/-0.20 mug/liter) obtained during ascorbic acid deficiency were not altered significantly after correction of the deficiency. Vasoconstrictor responses to intra-arterial norepinephrine and tyramine were augmented after vitamin repletion. During ascorbic acid deficiency, four subjects had reduced responsiveness of resistance vessels of the forearm to lower body negative pressure as compared to the responsiveness observed after vitamin repletion. Reflex tachycardia during lower body negative pressure and reflex bradycardia during the pressor responses to intravenous tyramine and norepinephrine were similar during the two studies. The results suggest that the decreased vascular responsiveness to intra-arterial norepinephrine and tyramine and to lower body negative pressure during ascorbic acid deficiency is caused by a defect in the ability of resistance vessels to constrict in response to adrenergic stimuli. Ascorbic acid deficiency in man does not interrupt autonomic reflexes and does not appear to cause significant depletion of endogenous norepinephrine.

Ascorbic Acid↗

PubMed1981

Evidence for central hypertyraminemia in hepatic encephalopathy.

In mongrel dogs, the effect of end-to-side portacaval shunt on plasma, cerebrospinal fluid (CSF) and brain tyramine, tyrosine, dopamine, norepinephrine, and epinephrine were studied. It was found that the level of tyramine in plasma, CSF, and selected brain regions increased steadily after the construction of the shunts. These elevations became more pronounced when the dogs manifested symptoms of hepatic encephalopathy. In postshunted dogs with stage II and III hepatic encephalopathy, tyramine concentration in corpus striatum (1,312 +/- 371), hypothalamus (400 +/- 67.0), and midbrain (660 +/- 78.7 ng/g) was significantly (P less than 0.05) higher than the level in dogs with stage 0 and I hepatic encephalopathy and sham-operated dogs serving as controls (corpus striatum, 831 +/- 140; hypothalamus, 167 +/- 40.0; and midbrain, 132 +/- 37.4 ng/g). This was followed by a concomitant depletion of dopamine and norepinephrine in these brain regions (postshunt: dopamine 104 +/- 20.0, 3,697 +/- 977, and 105 +/- 14.1; norepinephrine 521 +/- 71.6, 81.6 +/- 13.7, and 218 +/- 31.7 ng/g; vs. sham group: dopamine 532 +/- 83.1, 8,210 +/- 1,126, and 192 +/- 35.0; norepinephrine 1,338 +/- 425, 124 +/- 21.3, and 449 +/- 89.7 ng/g) of encephalopathic dogs with portacaval shunt. Furthermore, tyramine, tyrosine, dopamine, and norepinephrine levels in plasma and CSF increased markedly as clinical features in the dogs' behavior characteristic of hepatic encephalopathy occurred, including hypersalivation, ataxia, flapping tremor, somnolence, and coma. Cerebral hypertyraminemia and a defect in sympathetic neurotransmission may contribute to the development of hepatic encephalopathy of liver disease.

Animals↗

PubMed1983

Does lithium balance the neuronal bilateral asymmetries in cluster headache?

Pupil size was measured using a pupillograph, and an asymmetric responsiveness to tyramine, instilled bilaterally, was observed in asymptomatic cluster headache patients. Relatives of cluster headache patients showed an anisocoric mydriasis to tyramine, too. This asymmetry was caused by a less marked mydriatic response of one side which, in the cluster headache sufferers, corresponds to the symptomatic side. After three months of treatment with lithium carbonate (900 mg/die), a bilateral decrease of pupil size was noted, possibly due to a reduced sympathergic tone. After six months of continued treatment an unknown mechanism, likely adaptive in nature, attenuated the effect of lithium on pupil size. Lithium also induced a symmetric response to tyramine by increasing tyramine mydriasis on the symptomatic pupil while reducing it on the asymptomatic pupil. It is postulated that lithium improves cluster headache by correcting abnormal bilateral asymmetries in central neuronal systems which regulate autonomic function and pain sensitivity of the structures involved in the cluster attack.

Cluster Headache↗

PubMed1997

Impact of placental restriction on the development of the sympathoadrenal system.

We have investigated the impact of chronic restriction of placental function on circulating catecholamine concentrations and responses to the indirectly acting, sympathomimetic amine, tyramine, in the fetal sheep in late gestation. In 10 ewes, endometrial caruncles or placental placentation sites were removed before conception (placental restriction (PR) group). Fetal sheep in the PR group were hypoxemic throughout late gestation and growth-restricted (3.02 +/- 0.35 kg) when compared with control fetal sheep (4.30 +/- 0.29 kg; n = 8) at 140 d of gestation. Fetal plasma concentrations of noradrenaline and adrenaline were higher (p < 0.05) in the PR (7.06 +/- 3.17 pmol/mL and 2.89 +/- 2.01 pmol/mL, respectively) than in the control group (3.55 +/- 0.54 pmol/mL and 1.30 +/- 0.48 pmol/mL, respectively) throughout late gestation. Plasma noradrenaline, but not adrenaline concentrations, increased significantly between 110 and 140 d of gestation in both the PR and control group, and there was a significant inverse relationship between plasma noradrenaline and arterial PO2 in the PR and control groups (plasma noradrenaline = 12.34 - 0.40 PO2). In the PR group, plasma noradrenaline increased (p < 0.05) after tyramine infusion from 4.51 +/- 1.28 pmol/mL to a peak of 19.40 +/- 3.56 pmol/mL. In the control group, noradrenaline increased from 2.08 +/- 0.30 pmol/mL to a peak of 12.23 +/- 1.67 pmol/mL after tyramine infusion. There was no difference, however, in the maximal proportional changes in plasma noradrenaline concentrations in the PR (319 +/- 55%) and control (449 +/- 100%) groups after tyramine. We conclude that the most likely source of the increased plasma catecholamines in the PR group is enhanced catecholamine synthesis and secretion from developing sympathetic neurons.

Adrenal Glands↗

PubMed1990

Effect of enflurane on contractile reactivity in isolated canine mesenteric arteries and veins.

The effects of enflurane on responses of isolated canine mesenteric arteries and veins to transmural nerve stimulation and to exogenously administered norepinephrine (a mixed alpha 1- and alpha 2-adrenoceptor agonist), phenylephrine (a selective alpha 1-adrenoceptor agonist), and tyramine were studied. The contractile responses of the arteries and the veins to transmural nerve stimulation and to norepinephrine were attenuated by exposure to enflurane; the responses to phenylephrine were decreased more than those to norepinephrine. When compared with the effect of enflurane on transmural nerve stimulation-induced responses, exposure to enflurane resulted in slight attenuation of the contractile responses caused by tyramine, suggesting that enflurane may inhibit the responses to tyramine by interfering with an interaction between released norepinephrine and postjunctional alpha 1-adrenoceptors rather than with tyramine-induced norepinephrine release. The data are also consistent with the view that enflurane acts on sympathetic nerve endings to inhibit release of norepinephrine associated with electrical stimulation-induced nerve membrane depolarization.

Animals↗

PubMed1975

[Central action of beta-phenylethylamine derivatives. (4) Effects on spontaneous motor activity and body temperature of beta phenylethyamine derivatives injected into the brain in reserpine pretreated mice].

Effects on spontaneous motor activity and body temperature of beta-phenylethlamine derivatives injected into the cerebral ventricles in reserpine or reserpine and isocarboxazide pretreated mice were investigated with the following results. 1) Each injection of tyramine (40 mug) and dopamine (40 mug) increased the spontaneous motor activity measured by the photo-cell counters method in reserpinized mice. 2) Each injection of tyramine (40 mug), dopamine (40 mug) and beta-phenylethylamine (40 mug) increased the spontaneous motor activity measured by both the wheel cage and photo-cell counters methods in reserpine and isocarboxazide-pretreated mice, but noradrenaline (20 mug) and isoproterenol (80 mug) did not increase the spontaneous motor activity as determined by both methods. 3) The injection of tyramine (40 and 80 mug), dopamine (10 and 40 mug) and p-octopamine (40 mug) increased the body temperature in reserpine and isocarboxazide pretreated mice. 4) Tyramine, dopamine and p-octopamine caused a marked increase in the body temperature as compared with control injection in reserpine and isocarboxazide-pretreated mice, whereas isoproterenol had no influence on body temperature. Our results suggest that beta-phenylethylamine derivatives have different effects in reserpinized and non-pretreated states.

Animals↗

PubMed1977

[Studies on monoamine oxidase. (Report 37) Effects of oxygen concentration on rat liver and brain monoamine oxidase (author's transl)].

MAO activity in rat brain mitochondria with tyramine as substrate at 100% oxygen concentration was three times as much as that at 20%. When serotonin served as substrate, difference in activities between the two oxygen concentrations was not significant. Similar results were obtained when rat liver MAO was used as the enzyme source. At 100% oxygen concentration, pargyline showed the most potent inhibition of MAO activity in liver mitochondria with tyramine as substrate, but inhibitions caused by pheniprazine and harmaline were not remarkable. At 100% oxygen concentration, harmaline showed the most potent inhibition of MAO activity in the liver when serotonin served as substrate, while inhibitions of the MAO activity by pargyline and pheniprazine were weak. At 20% oxygen concentration, harmaline showed the most potent inhibition of MAO activity in the brain when serotonin was used as substrate. These inhibitions were studied using Lineweaver-Burk plots. Pargyline revealed a noncompetitive inhibition to MAO activity in liver and brain with tyramine and serotonin as substrate, harmaline a competitive inhibition to MAO activity in liver and brain with tyramine as substrate, while noncompetitive inhibition to MAO activity in liver and brain was evident when serotonin was used as the substrate.

Animals↗

PubMed1981

Studies on beta-phenylethylamine deamination by human placental monoamine oxidase.

Kinetical properties of human placental monoamine oxidase (MAO) were investigated in studies on inhibitors and mixed substrates. MAO activity was determined by a radioisotopic assay. Lineweaver-Burk plots were linear at higher and lower concentrations of PEA, whereas at intermediate substrate concentrations, a downward curving plot was obtained. The Km values of the low- and high-affinity sites for PEA deamination were estimated. Studies with mixed substrates showed that 5-HT was a competitive inhibitor and tyramine a mixed-type inhibitor of deamination at high concentrations of PEA, whereas both were non-competitive inhibitors at lower concentrations of PEA. After pre-incubation of human placental mitochondrial preparations with deprenyl, Lineweaver-Burk plots were completely linear, and the Km value was the same as that obtained at low concentrations of PEA in the absence of deprenyl. Tyramine and 5-HT were competitive inhibitors of PEA deamination by deprenyl-treated MAO. From these results it is concluded that there are two kinds of MAO with high- and low-affinity sites for PEA in mitochondria of human placenta, corresponding to type B and A Mao, and that tyramine, 5-HT and PEA share a substrate-binding site on type A Mao, while tyramine and 5-HT bind to a site on type B MAO that is different from the PEA binding site.

Deamination↗

PubMed1981

Effect of epinephrine and 5-hydroxytryptamine on in vitro thyroid iodine organification.

The effect of epinephrine (E) and 5-hydroxy-tryptamine (5-HT) on some elements involved in thyroid iodine organification was studied using a bovine thyroid subcellular fraction sedimented at 30 000 g. 131I-incorporation into particulate proteins and into tyrosine ws increased by 10(-3) M and 10(-5) M E and 5-HT. This effect was inhibited by 6-n-propyl-2-thiouracil and by catalase. In the presence of these amines the activity of NADPH-cytochrome c reductase was not modified. Both E and 5-HT were able to generate H2O2 when added to the particulate fraction as measured by the oxidation of o-dianisidine. H2O2 generation and [131I]iodotyrosine formation were inhibited by pargyline, a monoamine oxidase (MAO) inhibitor. Tyramine, a specific substrate for thyroid MAO, produced H2O2 and increased [131]iodotyrosine formation. This effect was higher when compared to the effect elicited by E or 5-HT. The stimulatory effects of tyramine were blocked by pargyline. The action of tyramine on H2O2 generation and [131I]iodotyrosine formation was diminished when E or 5-HT were incorporated to the system. From these results it suggested that E and 5-HT serving as MAO substrates would generate H2O2 and in this way increase the thyroid iodine organification. On the other hand, these amines would be able to reduce the increased H2O2 generation induced by tyramine and thus decrease the iodination process. These findings could explain the stimulatory or inhibitory effects of biogenic amines on thyroid function which are dependent on the previous thyroid activity.

Animals↗

PubMed1983

Increased systemic vascular responsiveness to catecholamines in spontaneously hypertensive rats.

Systemic vascular responsiveness to i.v. bolus injections of norepinephrine and tyramine was evaluated in adult male spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY). Changes in total peripheral resistance (TPR) were used as an index of vascular response. Dose-response curves were plotted with 1n-dose on the x-axis and percent of maximum change in TPR on the y-axis, and the following indices of responsiveness were used: slope, 1nED50, 1nx-intercept, and maximum response. Measurements were made before and after ganglionic blockade with pentolinium (5 mg/kg, i.v.). Cardiac output for TPR calculations was obtained from an implanted flow probe on the ascending aorta. The slopes and maximum responses to norepinephrine and tyramine were greater in SHR v. WKY, P less than .05, before and after pentolinium treatment. There were no significant differences in 1nED50 or 1nx-intercept between WKY and SHR for tyramine and norepinephrine prior to pentolinium. After pentolinium 1nED50 and 1nx-intercept were similar for SHR and WKY for norepinephrine, but were greater in SHR for tyramine. The results demonstrate an increased systemic vascular responsiveness to catecholamines in adult SHR, with no evidence of increased systemic vascular sensitivity. These findings are consistent with the concept of increased systemic vascular responsiveness to catecholamines in adult SHR secondary to structural changes in blood vessels.

Angiotensin II↗

PubMed1977

Differential effects of the isomers of tetramisole on adrenergic neurotransmission in cutaneous veins of dog.

Clinical observations indicate that dexamisole and levamisole, the isomers of tetramisole, cause mood elevation. Their effects on smooth muscle cells and adrenergic nerves were investigated in strips of dogs' saphenous veins. Dexamisole (2.5 X 10(-6) to 4 X 10(-5) M) augmented the contractile response to norepinephrine but depressed that to tyramine; cocaine inhibited the augmentation of the norepinephrine response. Levamisole (10(-5) M) did not alter the response to norepinephrine, but augmented that to tyramine. At 1.6 X 10(-4) M dexamisole, more than levamisole, depressed the responses to norepinephrine, tyramine and acetylcholine. Activation by K+ ions was not affected by the isomers. Preparations, incubated with 3H-norepinephrine, were mounted for superfusion, tension recording and determination of 3H-norepinephrine and metabolites in the superfusate. Dexamisole and levamisole augmented the 3H-norepinephrine overflow during nerve stimulation; levamisole decreased the efflux of deaminated metabolites. During tyramine-induced contractions, dexamisole depressed and levamisole augmented the efflux of 3H-norepinephrine; they reduced the appearance of metabolites. The increases in 3H-norepinephrine caused by the isomers during nerve stimulation were not seen after phenoxybenzamine. Dexamisole, more than levamisole, inhibited tissular uptake of 3H-norepinephrine. Levamisole, more than dexamisole, inhibited monoamine oxidase activity in vein homogenates. These interferences with release and disposition of norepinephrine may be related to the antidepressant properties of the tetramisole isomers.

Acetylcholine↗

PubMedDate not supplied

[Production of non-volatile amines by strains of enterococci].

During the last few years there has been great interest concerning the problems related with the presence of pressor amines in different kinds of cheese, specially since the "cheese syndrome" was made evident. Since the capacity of the bacterial groups involved in cheese manufacture to produce these amines has not yet been clarified, it was decided to study the production capacity of tyramine, tryptamine and histamine of enterococci strains probably used in the starter cultures. Forty-one enterococci strains were analysed cultivating them in milk and in milk with the addition of the corresponding aminoacids. It was determined that only low percentages of Streptococcus faecalis subsp. liquefaciens and Streptococcus durans strains (34% and 11% respectively) produced traces of tyramine and tryptamine in milk. But when cultivated in the presence of the corresponding aminoacids, a large percentage of strains of all the species produced tyramine in high concentrations and different percentages of them produced tryptamine in concentrations no higher than 200 ppm. All strains analysed proved to be unable to produce histamine. It can be concluded that there exists a strong probability for enterococci to produce tyramine and tryptamine in different concentrations specially when developed in the presence of the corresponding aminoacids.

Amino Acids↗