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PubMed2001

Amphetamine, 3,4-methylenedioxymethamphetamine, lysergic acid diethylamide, and metabolites of the catecholamine neurotransmitters are agonists of a rat trace amine receptor.

The trace amine para-tyramine is structurally and functionally related to the amphetamines and the biogenic amine neurotransmitters. It is currently thought that the biological activities elicited by trace amines such as p-tyramine and the psychostimulant amphetamines are manifestations of their ability to inhibit the clearance of extracellular transmitter and/or stimulate the efflux of transmitter from intracellular stores. Here we report the discovery and pharmacological characterization of a rat G protein-coupled receptor that stimulates the production of cAMP when exposed to the trace amines p-tyramine, beta-phenethylamine, tryptamine, and octopamine. An extensive pharmacological survey revealed that psychostimulant and hallucinogenic amphetamines, numerous ergoline derivatives, adrenergic ligands, and 3-methylated metabolites of the catecholamine neurotransmitters are also good agonists at the rat trace amine receptor 1 (rTAR1). These results suggest that the trace amines and catecholamine metabolites may serve as the endogenous ligands of a novel intercellular signaling system found widely throughout the vertebrate brain and periphery. Furthermore, the discovery that amphetamines, including 3,4-methylenedioxymethamphetamine (MDMA; "ecstasy"), are potent rTAR1 agonists suggests that the effects of these widely used drugs may be mediated in part by this receptor as well as their previously characterized targets, the neurotransmitter transporter proteins.

Amino Acid Sequence↗
PubMed1963

Studies on coccidioides immitis. II. Physiological studies on in vitro spherulation.

Brooks, Lula D. (Arizona State University, Tempe) and William T. Northey. Studies on Coccidioides immitis. II. Physiological studies on in vitro spherulation. J. Bacteriol. 85:12-15. 1963.-Studies on the amino acids assayed in Edamine revealed that the amino acids phenylalanine, tyrosine, and tryptophan, in addition to the amino acid derivatives dihydroxyphenylalanine (DOPA), epinephrine, tyramine monohydrochloride (tyramine HCl), and pyrocatechol play an important role in the Coccidioides immitis conversion process. In the presence of phenylalanine, tyrosine, tryptophan, DOPA, pyrocatechol, dextrose, and biotin, conversion as well as maturation was demonstrated. However, in epinephrine and tyramine HCl combinations, conversion occurred without maturation of the spherules. The availability of increased amounts of melanin precursors is suggested as a possible explanation for the increased susceptibility of the dark-skinned races to disseminated coccidioidomycosis. Conversion and maturation were also noted when lactic and fumaric acids served as carbon sources. The conversion of a limited number of arthrospores to spherules and their subsequent maturation in the presence of only phenol and biotin suggest the possibility that the key to the C. immitis conversion process lies in the availability of certain ring structures.

Biotin↗
PubMed2001

Analysis of bacterial vaginosis-related amines in vaginal fluid by gas chromatography and mass spectrometry.

The presence of various amines in vaginal fluid from women with malodorous vaginal discharge has been reported before. The investigations have used several techniques to identify the amines. However, an optimized quantification, together with a sensitive analysis method in connection with a diagnostic procedure for vaginal discharge, including the syndrome of bacterial vaginosis, as defined by the accepted "gold standard," has not been done before. We now report a sensitive gas chromatographic and mass spectrometric method for identifying the amines isobutylamine, phenethylamine, putrescine, cadaverine, and tyramine in vaginal fluid. We used weighted samples of vaginal fluid to obtain a correct quantification. In addition, a proper diagnosis was obtained using Gram-stained smears of the vaginal fluid that were Nugent scored according to the method of Nugent et al. (R. P. Nugent et al., J. Clin. Microbiol., 29:297-301, 1991). We found that putrescine, cadaverine, and tyramine occurred in high concentrations in vaginal fluid from 24 women with Nugent scores between 7 and 10. These amines either were not found or were found only in very low concentrations in vaginal fluid from women with Nugent scores of 0 to 3. There is a strong correlation between bacterial vaginosis and the presence of putrescine, cadaverine, and tyramine in high concentrations in vaginal fluid.

Adult↗
PubMed2006

Alpha-Adrenergic receptor responsiveness is preserved during prolonged exercise.

Our laboratory has previously reported a decline in sympathetic nervous system restraint of skeletal muscle blood flow during prolonged mild-intensity exercise. This decline may be explained by a decrease in alpha(1)- and alpha(2)-adrenergic receptor responsiveness over time. Thus the purpose of the present study was to investigate the effect of exercise duration on alpha(1)- and alpha(2)-adrenergic receptor responsiveness during prolonged constant-load exercise. Mongrel dogs (n = 6) were instrumented chronically with transit-time flow probes on the external iliac arteries and an indwelling catheter in a branch of the femoral artery. On separate days, flow-adjusted doses of selective alpha(1)- (phenylephrine) alpha(2)-adrenergic-receptor (clonidine) agonists, and tyramine (to evoke endogenous norepinephrine release) were infused following 5, 30 and 50 min of mild-intensity treadmill exercise (3 miles/h), with hindlimb blood flow (HBF) and mean arterial pressure (MAP) monitored continuously. Vascular conductance (VC) was calculated as HBF/MAP. While the dogs ran on the treadmill at 3 miles/h, infusion of phenylephrine resulted in similar decreases in VC after 5 [73% (SD 10)], 30 [76% (SD 9)], and 50 [73% (SD 10)] min of exercise. Infusion of the alpha(2)-agonist clonidine also produced similar decreases in VC after 5 [58% (SD 10)], 30 [58% (SD 11)], and 50 [53% (SD 12)] min of exercise. Infusion of tyramine resulted in similar decreases in VC after 5 [55% (SD 15)], 30 [51% (SD 10)], and 50 [50% (SD 7)] min of exercise. These results demonstrate that alpha(1)- and alpha(2)-adrenergic receptor responsiveness to infusion of selective alpha(1)- and alpha(2)-adrenergic-receptor agonists and endogenous norepinephrine release (tyramine) does not decline during prolonged mild-intensity exercise. Thus a decrease in alpha-adrenergic receptor responsiveness over time does not appear to be responsible for the decrease in sympathetic restraint of muscle blood flow during prolonged exercise.

Adaptation, Physiological↗
PubMed2003

Functional mapping of rbOCT1 and rbOCT2 activity in the S2 segment of rabbit proximal tubule.

A strategy was developed to determine the distribution of activity mediated by the organic cation (OC) transporters OCT1 and OCT2 in rabbit renal proximal tubule (RPT). Both transporters displayed similar affinities for tetraethylammonium (TEA; in CHO-K1 cells, TEA concentrations that resulted in half-maximal transport were 19.9 and 34.5 microM for OCT1 and OCT2, respectively). Similarly, some OCs showed little capacity to discriminate between the two processes (IC50 values for ephedrine of 13.6 and 24.2 microM for OCT1 and OCT2, respectively). However, OCT2 had a higher affinity for cimetidine and [2-(4-nitro-2,1,3-benzoxadiazol-7-yl) aminoethyl]trimethylammonium (NBD-TMA; 1.3 and 1.4 microM, respectively) than did OCT1 (97.3 and 108 microM, respectively). Conversely, OCT1 had a higher affinity for tyramine and pindolol than did OCT2 (21.2 and 2.4 vs. 361 and 50 microM, respectively). We designated these as "discriminatory inhibitors" and used them to determine the relative contribution of OCT1 and OCT2 for TEA transport in single S2 segments of rabbit RPT. Cimetidine and NBD-TMA were high-affinity inhibitors of TEA transport in S2 segments (median IC50 values of 12.3 and 1.4 microM, respectively); in comparison, tyramine and pindolol were low-affinity inhibitors (265 and 69.3 microM, respectively). These IC50 values were sufficiently close to those for OCT2 to support the conclusion that TEA transport in the S2 segment of rabbit RPT is dominated by OCT2. However, the profile of inhibition of tyramine (an OCT1-selective substrate) transport in single S2 segments indicated that, despite a comparatively low level of expression, OCT1 can play a dominant role in the uptake of selected OC substrates.

Animals↗
PubMed1988

Differential effects of verapamil, nicardipine and diltiazem on Ca2+-dependent and Ca2+-independent noradrenaline release and contraction in isolated canine saphenous veins.

We reported that verapamil, nicardipine and diltiazem inhibited both 3H overflow and contraction induced by transmural nerve stimulation (TNS) in the canine saphenous vein preloaded with 3H-noradrenaline. In the present study, the effects of these Ca channel antagonists in the presence of tetraethylammonium (TEA) were investigated to evaluate whether the antagonists act by inhibiting Ca2+ influx into the nerve endings. The effects of the drugs on both responses to tyramine were also studied. In the 1 mmol/l-TEA-pretreated veins, verapamil and nicardipine inhibited only the contraction. Diltiazem inhibited the two parameters, the effects being nearly equipotent to those in the absence of TEA. The L-cis isomer of diltiazem inhibited the TNS-evoked responses to a similar degree as diltiazem, which was unaffected by 1 mmol/l TEA. Verapamil, nicardipine and diltiazem inhibited the TNS-evoked 3H overflow in 0.25 mmol/l Ca2+ and 20 mmol/l TEA medium, the inhibitions by the two former antagonists being greater than those seen in normal Krebs solution. TEA (1 mmol/l) added after the Ca channel antagonists, overcame the inhibition of the evoked overflow by diltiazem more poorly than that by verapamil or nicardipine. Only verapamil inhibited both responses to tyramine. These data together with previous results suggest that unlike verapamil and nicardipine, diltiazem may inhibit the TNS-evoked neurotransmitter release via a mechanism being unrelated to its Ca2+ influx-inhibiting action, resulting in an inhibition of the contraction, and that only verapamil inhibits the tyramine-evoked neurotransmitter release.

Animals↗
PubMed1992

Effect of chronic renal failure with and without secondary hyperparathyroidism on the activities of synaptosomal tyrosine hydroxylase and monoamine oxidase.

Norepinephrine (NE) content, release and uptake by brain synaptosomes are reduced in chronic renal failure (CRF), and this has been attributed to the state of secondary hyperparathyroidism. The decrease in NE content in CRF could not be explained by changes in NE uptake or release since in normal circumstances, NE content usually remains unchanged despite fluctuation in NE uptake and release. Since NE content is determined by its production and degradation, we examined the effect of CRF with and without excess parathyroid hormone (PTH) on the Michaelis-Menton constant (Km) and Vmax of tyrosine hydroxylase (TH), the rate-limiting enzyme for NE production, and monoamine oxidase (MAO), an enzyme involved in NE degradation of brain synaptosomes. Brain synaptosomes from rats with a 21-day CRF have a significantly (p less than 0.01) lower Vmax of TH (39.5 +/- 5.3 pmol tritiated H2O/mg protein/min) than that of normal rats (61. +/- 7.5 pmol tritiated H2O/mg protein/min) and a higher Km of MAO (59 +/- 2.9 nM tyramine) than normal animals (46 +/- 1.7 nM tyramine). Parathyroidectomy (PTX) in CRF rats normalized Vmax of TH (54 +/- 4.5 pmol tritiated H2O/mg protein) and Km of MAO (48.4 +/- 2.3 nM tyramine). Cytosolic calcium, [Ca2+]i, in brain synaptosomes is significantly (p less than 0.01) higher in rats with CRF (488 +/- 8.5 nM) than in normal (355 +/- 6.0 nM) or PTX-CRF (360 +/- 8.1 nM) rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Role of prostaglandins and kinins in the renal pressor reflex.

In previous studies we identified an afferent renal nerve-dependent pressor reflex elicited by acute unilateral renal artery stenosis (50% decrease in renal blood flow) in conscious, instrumented rats with reduced responsiveness of arterial baroreceptor reflexes and the renin-angiotensin system. The pressor reflex involves a neurogenic increase in peripheral resistance. The present study examined the nature of the intrarenal stimulus underlying this renal pressor reflex. Rats were subjected to sinoaortic denervation and, 7 to 10 days later, were chronically instrumented with Doppler flow probes on the right renal artery, superior mesenteric artery, and abdominal aorta and with an occluder on the right renal artery. Following surgical recovery and inhibition of the renin-angiotensin system (captopril), animals received intravenous isotonic saline, 6% of body weight over 60 minutes. Saline infusion did not alter baseline hemodynamics, vascular neurogenic tone, or responsiveness to tyramine, but it attenuated the reflex by 70%. A second series of experiments examined a possible role for intrarenal prostaglandins, kinins, or adenosine in the activation of renal sensory receptors during renal stenosis. Prostaglandin inhibition with intravenous administration of indomethacin and meclofenamate virtually abolished the reflex in the face of enhanced tyramine responsiveness, whereas kallikrein inhibition (aprotinin) attenuated the reflex pressor response by 33%. Adenosine inhibition with aminophylline or adenosine deaminase had no effect on the reflex; these agents and aprotinin did not affect vascular neuroeffector responsiveness (tyramine). The data suggest that the renal pressor reflex may be mediated by renal sensory nerves, possibly chemoreceptors, whose activation could depend on renal excretory function and synthesis of prostaglandins and kinins.

Adenosine↗
PubMed1980

Effect of salts on mitochondrial monoamine oxidase from bovine liver.

The effects of various salts on the activity of mitochondrial monoamine oxidase (MAO) from bovine liver were studied by measuring the initial and long-term enzyme reactions with an oxygen electrode and Warburg's manometer, respectively, using several monoamines as substrates. Salts with a -Cl- group, such as KCl and NaCl, or with a -NO3- group, such as KNO3 and NaNO3, increased the initial MAO activity with tyramine as substrate. NaCl strongly inhibited the long-term enzyme reaction. With tyramine as substrate, NaCl increased the activity only during the first 6 to 7 min of the reaction. Similarly with beta-phenylethylamine or butylamine as substrate, NaCl increased the initial MAO activity, but decreased the activity in the long-term reaction. On the other hand, with serotonin or benzylamine as substrate, NaCl decreased both the the initial reaction and the long-term reaction. The effect of NaCl on the enzyme with tyramine as substrate was reversible, while with serotonin as substrate it was irreversible. These results indicate that the effect of NaCl depends on the substrate used and suggest that bovine liver mitochondria contain at least two different forms of MAO.

Animals↗
PubMed1984

Some interrelated properties of A and B form monoamine oxidase in monkey brain mitochondria.

The multiplicity of monoamine oxidase (MAO) in monkey brain was studied by comparing the relationship between the selective substrates of MAO and the pH-activity curves obtained using these substrates. When mitochondrial and A-form MAO were used as the enzyme preparations with serotonin (5-HT) and norepinephrine (NE), preferential substrates for A-form MAO, the pH optima were 8.8 and 7.8 with 5-HT and 8.5 and 7.2 with NE. These substrates were also oxidized by B-form MAO after changing the pH of the incubation medium (shift to alkaline); these pH optima were 9.0 and 8.2, respectively. When common substrates of MAO were used (tyramine, octopamine, dopamine and tryptamine), the pH activity curves obtained were all broad and bell-shaped with pH optima for the 3 species of enzyme (mitochondria, A-form and B-form MAO) at 8.0, 7.8, and 8.0 with tyramine; 8.3, 7.5, and 8.5 with octopamine; 7.8, 7.5, and 8.5 with dopamine; and 8.0, 8.3, and 6.9 with tryptamine, respectively. The pH optima were 6.6 with beta-phenylethylamine (beta-PEA) and 9.0 with benzylamine, preferential substrates for B-form MAO, for either mitochondria or B-form MAO. The Km values obtained for tryptamine and beta-PEA were lower than those for the other substrates of MAO, regardless of the enzyme preparations. The Km and Vmax values of both forms MAO for 5-HT and NE were similar to those of the A-form MAO. The differences in the Km and Vmax values of the A-form MAO and B-form MAO for common substrates were comparable. Tyramine, octopamine and dopamine were substrates for both forms MAO, with only a slight preference for B-form MAO over A-form MAO. However, tryptamine may be deaminated predominantly by A-form MAO.

Animals↗
PubMed1996

Monoamine oxidase inhibitors. An update on drug interactions.

After initial enthusiasm, the use of monoamine oxidase inhibitors (MAOIs) has been limited by the wide range of MAOI-drug and MAOI-food interactions that are possible, particularly with sympathomimetic medications or tyramine-containing foods, resulting in hypertensive reactions. Despite their clinical benefits, this has led to a reduction in use of such medications. Discovery of the 2 main subgroups of monoamine oxidase, types A and B, led to the synthesis of MAOIs selective for one or other of these isoenzymes. Consequently, selegiline (deprenyl), a selective MAO-B inhibitor, was developed for the treatment of idiopathic Parkinson's disease. This drug is useful in the treatment of the early stages of the disease and later on as an adjunct to other drug therapies. Although the selective MAO-A inhibitor, clorgiline (clorgyline), was found to be effective in the treatment of depression, it still retained the potential to cause hypertensive reactions. Recently, agents that are not only selective, but reversible in their inhibition of MAO-A (RIMAs) have been synthesised (e.g. moclobemide and toloxatone), and have proven antidepressant efficacy. Whilst they are less likely to induce hypertensive reactions with the concomitant administration of sympathomimetic drugs or with tyramine-rich foodstuffs, it still seems wise to advocate care in co-prescribing potentially interacting medications and to advise a degree of caution with regard to the dietary intake of foodstuffs likely to contain a high tyramine content. Although these newer drugs represent an advance in safety, their use has, as yet, only been established in the treatment of depression. RIMAs also retain a potential for adverse interaction with other drugs. Concomitant prescription of serotonin-enhancing drugs should only be undertaken with caution for patients on moclobemide, toloxatone or selegiline. Coprescription of sympathomimetic drugs should also be avoided with these newer MAOIs and patients should be advised against purchasing over-the-counter preparations that may contain sympathomimetic drugs.

Animals↗
PubMed1992

An Australian multicentre study of moclobemide versus amitriptyline in the treatment of depression.

This paper reports the results of a multicentre study of the new monoamine oxidase inhibitor, moclobemide, in the treatment of major depression. Moclobemide is a specific monoamine oxidase-A inhibitor which does not bind irreversibly to the enzyme, unlike the currently available MAOIs. Recent studies would suggest that in subjects taking moclobemide blood pressure elevation caused by tyramine is significantly less than that induced by the irreversible MAOIs, particularly when tyramine is administered in an oral form. Forty-eight patients with major depression were randomly allocated to treatment with either moclobemide or amitriptyline for 4 weeks in a double-blind comparison. There were no statistically significant differences between the two groups on measures of efficacy. Patients taking amitriptyline reported a greater number of side-effects and more patients in the amitriptyline group dropped out because of these. There were no reports of interactions with tyramine-containing foods.

Adult↗
PubMed1994

Mechanism of decrease in heart rate by peripheral dopaminergic D2-receptors.

We performed this study in order to verify the heart rate decrease caused by the D2-receptor on cardiac sympathetic nerve endings and its relation to the concentration of norepinephrine in synaptic clefts. Sprague-Dawley rats were pithed and the heart rate was increased either by electrical stimulation of the cardiac accelerator nerve or by intravenous infusion of norepinephrine, tyramine, or isoproterenol. Increased heart rate by electrical stimulation of cardiac accelerator nerve was dose-dependently lowered by lisuride and its effect was blocked by pretreatment with sulpiride but not with yohimbine and SCH 23390. Also, the heart rate was decreased in a dose-dependent manner by clonidine and this effect was blocked by pretreatment with yohimbine, but not with sulpiride. For increased heart rate by infusion of norepinephrine, tyramine, or isoproterenol, the heart rate lowering effect of lisuride was more marked in the norepinephrine-and tyramine-infusion groups, in which the intrasynaptic concentration of norepinephrine was elevated, compared to the isoproterenol-infusion group, in which intrasynaptic concentration of norepinephrine was not elevated. In conclusion, there is a D2-receptor on the cardiac sympathetic nerve endings which decreases the heart rate and is different from the presynaptic alpha 2-receptor. Also, the heart rate lowering effect via stimulation of the D2-receptor by lisuride was more marked with increased concentration of norepinephrine in the synaptic cleft.

Animals↗
PubMed2004

Biogenic amine formation and "zapatera" spoilage of fermented green olives: effect of storage temperature and debittering process.

The effects of temperature and the debittering process on amine formation and other chemical changes related to "zapatera" spoilage of fermented green table olives during storage, without any chemical correction, were studied. Unwashed olive brines were more concentrated in all analyzed compounds, except NaCl. No changes in formic, acetic, and succinic acids or in ethanol, hydroxytyrosol, or tyrosol were observed in the olive brines during storage. The concentration of putrescine in the brine at the beginning of storage and end of fermentation was about 38 mg/liter, and it did not change during storage. This amine only seems to be produced during the active fermentation phase. The effects of temperature and the type of debittering process and time and its interactions (except the time x temperature x debittering process on pH) had significant effects on the production of cadaverine and tyramine, as well as on changes of pH and lactic and propionic acids. Storage at 15 degrees C produced a complete stabilization of the fermented olives. However, storage of washed olives at 20 and 28 degrees C produced a gradual decrease of lactic acid content, an increase in pH, production of propionic acid, and formation of cadaverine and tyramine, the effect becoming greater as the temperature rose. It appears that formation of cadaverine and tyramine only occurs during storage and might be related to zapatera spoilage. Changes were always significantly lower in unwashed olives, which leads to a practical stabilization of the product.

Biogenic Amines↗
PubMed2004

Relation of biogenic amines with microbial and sensory changes of whole and filleted freshwater rainbow trout (Onchorynchus mykiss) stored on ice.

The biogenic amine (BA) content of whole and filleted rainbow trout was monitored during ice storage for a period of 18 days and related to respective microbial and sensorial changes occurring during the same period. Eight amines, namely, putrescine, cadaverine, tyramine, spermidine, tryptamine, beta-phenylethylamine, spermine, and histamine, were determined. Agmatine was not detected in any of the fish samples. In all cases, concentration of BAs was higher (P < 0.05) in filleted compared with whole trout samples. Pseudomonads, H2S-producing bacteria, and, to a lesser extent, Enterobacteriaceae were the dominant microorganisms in both whole and filleted trout. Higher populations (P < 0.05) of these microorganisms were present in filleted trout compared with whole fish samples. Of the BAs determined, concentration of putrescine, cadaverine, spermidine, tryptamine, and beta-phenylethylamine increased steeply in both whole and filleted trout between days 15 and 18 of storage when pseudomonads and H2S-producing bacteria reached approximately 10(6) to 10(7) CFU/g. For the rest of the BAs, including tyramine, histamine, and spermine, a stepwise increase was recorded throughout the entire storage period. Interestingly, Enterobacteriaceae counts remained below 10(6) throughout the entire storage period, accounting for the lower production of histamine. A putrescine value of 13 to 14 mg/kg and a spermidine value of approximately 7 mg/kg for both the whole and filleted trout obtained after 12 and 9 days, respectively, may be proposed as the upper limit for spoilage initiation (freshness indicator) of fresh rainbow trout based on sensorial and microbiological (total viable count of 10(6) to 10(7)) data. With respect to other amines determined, both tyramine and spermine may also be proposed as freshness indicators preferably for whole trout, whereas tryptamine, beta-phenylethylamine, histamine, and cadaverine produced only during later stages of storage are not suitable as freshness indicators of either whole or filleted trout.

Animals↗
PubMed2001

Reappearance of cardiac presynaptic sympathetic nerve terminals in the transplanted heart: correlation between PET using (11)C-hydroxyephedrine and invasively measured norepinephrine release.

UNLABELLED: Previously, sympathetic reinnervation of the transplanted heart has been described using invasive catheterization techniques and noninvasive radionuclide imaging techniques. However, little is known about the agreement between these 2 methods. Thus, correlation between (11)C-hydroxyephedrine (HED) PET and invasively measured norepinephrine (NE) release was investigated in transplant recipients in this study. METHODS: Using PET and the catecholamine analog HED, 17 patients were studied between 2 mo and 13.6 y after transplantation. Based on results in completely denervated hearts, areas with HED retention >7%/min were defined as reinnervated. Additionally, transcardiac NE release induced by intravenous tyramine (55 microg/kg) was measured by coronary sinus and aortic catheterization within 1 wk of the PET study. NE levels between coronary sinus and aortic root, DeltaNE(CS-AO), were calculated at baseline and after tyramine administration. Differences of more than 3 SD of baseline (>163 pg/mL) were interpreted as reinnervation. RESULTS: HED retention indicated reinnervation in 10 patients. Maximal HED retention ranged from 4.3%/min to 16.4%/min. DeltaNE(CS-AO) 1 min after tyramine administration ranged between -10 pg/mL and 1157 pg/mL, and 8 patients were above the reinnervation threshold. Fisher's exact test demonstrated good agreement between results of PET and DeltaNE(CS-AO) measurements (P = 0.002). Maximal HED retention was also significantly correlated with NE release (r = 0.69; P = 0.001). CONCLUSION: Results of invasively measured NE release and noninvasive (11)C-HED PET are well correlated. This study further supports the usefulness of PET as a noninvasive approach for detection of reappearance of catecholamine uptake sites after heart transplantation.

Adrenergic Fibers↗
PubMedDate not supplied

[Effect of biogenic amines on glycogen degradation in isolated rat hepatocytes].

Serotonin and tyramine affected dissimilarly the enzyme activity involved in degradation of glycogen in isolated rat hepatocytes. Serotonin inhibited hydrolytic enzymes acid alpha-glucosidase, alpha-amylase and amylo-1,6-glucosidase but activated phosphorylase inducing a decrease of glycogen content in cells. Tyramine inhibited acid alpha-glucosidase and amylo-1,6-glucosidase, did not affect the alpha-amylase and phosphorylase activities and increased content of glycogen in cells. Tyramine may be used as stimulator of glycogen accumulation in liver cells.

Animals↗
PubMed1992

New inhibitors of sepiapterin reductase. Lack of an effect of intracellular tetrahydrobiopterin depletion upon in vitro proliferation of two human cell lines.

N-Acetylserotonin (compound 1) and N-acetyldopamine (compound 7) inhibit bovine adrenal medullary sepiapterin reductase in a manner competitive with the pterin substrate and have Ki values of 0.12 and 0.4 microM, respectively. Molecular modeling suggests that the phenyl rings of the two compounds bind in the pyrimidine pocket of the enzyme with the 3-hydroxyl of dopamine or the 5-hydroxyl of serotonin aligned at the pyrimidine 4-position. Further, the acetyl moieties of the two inhibitors appear to mimic the substrate side chain. Consistent with this analysis, N-acetyl-m-tyramine (compound 13) is also an excellent competitive inhibitor (Ki = 0.13 microM), whereas N-acetyltryptamine (compound 2), N-acetyl-p-tyramine (compound 14) and N-acetylphenylethylamine (compound 15) all bind poorly. Interestingly, restricted-rotation analogs of N-acetyldopamine and N-acetyl-m-tyramine are noncompetitive inhibitors of the enzyme. Modification of N-acetyldopamine to N-chloroacetyldopamine (compound 10) or of N-acetylserotonin to the N-chloroacetyl (5) or N-methoxyacetyl (compound 6) analogs results in greatly increased competitive affinity, with Ki = 0.014 microM for the dopamine analog and 0.006 and 0.008 microM, respectively, for the serotonin analogs. In MOLT-4 T-cell leukemia and MCF-7 breast adenocarcinoma in culture, 0.1 mM N-methoxyacetylserotonin depleted tetrahydrobiopterin by greater than or equal to 97 and greater than 50%, respectively, with no effect upon cell growth. In both cell lines, the GTP cyclohydrolase inhibitor, 2,4-diamino-6-hydroxypyrimidine at 1-5 mM also depleted tetrahydrobiopterin greater than or equal to 97%. In this case, however, modest growth inhibition did occur. Since the growth inhibition could not be reversed upon tetrahydrobiopterin repletion, inhibition was due to other effects of the inhibitor rather than to tetrahydrobiopterin depletion. The results show that there is no effect on cell growth when at least 97% of the tetrahydrobiopterin in these cell lines is depleted. Since the sepiapterin reductase inhibitor depleted tetrahydrobiopterin with fewer nonspecific effects than the cyclohydrolase inhibitor, it will be useful for determining metabolic effects of tetrahydrobiopterin depletion.

Alcohol Oxidoreductases↗