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PubMed1977

Genetic control of arylsulfatase synthesis in Klebsiella aerogenes.

It was shown that at least four genes are specifically responsible for arylsulfatase synthesis in Klebsiella aerogenes. Mutations at chromosome site atsA result in enzymatically inactive arylsulfatase. Mutants showing constitutive synthesis of arylsulfatase (atsR) were isolated by using inorganic sulfate or cysteine as the sulfur source. Another mutation in which repression of arylsulfatase by inorganic sulfate or cysteine could not be relieved by tyramine was determined by genetic analysis to be on the tyramine oxidase gene (tyn). This site was distinguished from the atsC mutation site, which is probably concerned with the action or synthesis of corepressors of arylsulfatase synthesis. Genetic analysis with transducing phage PW52 showed that the order of mutation sites was atsC-atsR-atsA-tynA-tynB. On the basis of these results and previous physiological findings, we propose a new model for regulation of arylsulfatase synthesis.

Amino Acid Oxidoreductases↗

PubMed1981

Stimulation of bacterial arylsulfatase activity by arylamines: evidence for substrate activation.

A number of arylamines (including tyramine and tryptamine) increased the in vitro activity of arylsulfatase from Pseudomonas sp. strain C12B. Amino acid analogs of these amines (e.g., tyrosine and tryptophan) failed to exert an effect. Stimulation of activity by tyramine could not be accounted for in terms of sulfotransferase activity for this phenol, and no shift in the pH optimum for the enzyme occurred in the presence of tryptamine. Increased Vmax due to these amines was independent of enzyme concentration but varied significantly with substrate concentration. Evidence is presented which suggests that arylamines enhance arylsulfatase activity by forming a salt linkage with the substrate and rendering it more susceptible to enzymatic and acid-catalyzed hydrolyses. The recrystallized tryptamine salt of the substrate exhibited a reduced affinity for the enzyme but was hydrolyzed more rapidly than the potassium salt, which is normally employed as the assay substrate.

Arylsulfatases↗

PubMed1992

A monoamine-regulated Klebsiella aerogenes operon containing the monoamine oxidase structural gene (maoA) and the maoC gene.

The Klebsiella aerogenes gene maoA, which is involved in the synthesis of monoamine oxidase, was induced by tyramine and the related compounds, subjected to catabolite and ammonium ion repression, and cloned. The nucleotide sequence of the region involved in monoamine oxidase synthesis was determined. Two open reading frames, the maoA gene and a hitherto unknown gene (maoC), were found. These are located between a potential promoter sequence and a transcriptional terminator sequence. A region of the Escherichia coli chromosome that was highly homologous to the Klebsiella maoA gene was found. The potential maoA gene is located at 30.9 min on the E. coli chromosome. Analysis of the amino acid sequences of the first 11 amino acids from the N terminus of the purified monoamine oxidase agrees with those deduced from the nucleotide sequence of the maoA gene. The leader peptide extends over 30 amino acids and has the characteristics of a signal sequence. Primer extension and S1 nuclease mapping of transcripts generated in vivo suggests that the tyramine-induced mRNA starts at a site 62 bases upstream from the ATG initiation codon of the maoC gene. In the putative promoter region, a high degree of similarity to the consensus sequence for the binding site of cyclic AMP receptor protein was found. Thus, the mao region is composed of two cistrons, and the mao operon is regulated by monoamine compounds, glucose, and ammonium ions.

Amino Acid Sequence↗

PubMed2006

The mechanism of the tyrosine transporter TyrP supports a proton motive tyrosine decarboxylation pathway in Lactobacillus brevis.

The tyrosine decarboxylase operon of Lactobacillus brevis IOEB9809 contains, adjacent to the tyrosine decarboxylase gene, a gene for TyrP, a putative tyrosine transporter. The two genes potentially form a proton motive tyrosine decarboxylation pathway. The putative tyrosine transporter gene of L. brevis was expressed in Lactococcus lactis and functionally characterized using right-side-out membranes. The transporter very efficiently catalyzes homologous tyrosine-tyrosine exchange and heterologous exchange between tyrosine and its decarboxylation product tyramine. Tyrosine-tyramine exchange was shown to be electrogenic. In addition to the exchange mode, the transporter catalyzes tyrosine uniport but at a much lower rate. Analysis of the substrate specificity of the transporter by use of a set of 19 different tyrosine substrate analogues showed that the main interactions between the protein and the substrates involve the amino group and the phenyl ring with the para hydroxyl group. The carboxylate group that is removed in the decarboxylation reaction does not seem to contribute to the affinity of the protein for the substrates significantly. The properties of the TyrP protein are those typical for precursor-product exchangers that operate in proton motive decarboxylation pathways. It is proposed that tyrosine decarboxylation in L. brevis results in proton motive force generation by an indirect proton pumping mechanism.

Amino Acid Transport Systems↗

PubMed1997

Sympathetic reinnervation and heart rate variability after cardiac transplantation.

BACKGROUND: Heart rate variability is thought to measure autonomic modulation, but the relation has never been demonstrated directly in humans. AIM: To test the hypothesis that increased low frequency heart rate variability reflects sympathetic reinnervation after cardiac transplantation. PATIENTS: 24 cardiac transplant recipients at the time of routine surveillance coronary angiography two or more years after cardiac transplantation, and 10 controls with normal coronary arteries undergoing angiography for investigation of chest pain. SETTING: Regional cardiothoracic centre. METHODS: Sympathetic effector function at the sinus node was assessed by measuring the fall in cycle length for two minutes after injection of tyramine to the artery supplying the sinus node. Heart rate variability was measured from three-minute RR interval sequences at rest, during metronomic respiration, and before and after atropine. RESULTS: The logarithm of the low frequency component of heart rate variability during metronomic respiration was linearly related to the logarithm of the change in cycle length after injection of tyramine (R2 = 0.28, P = 0.007). Absolute units more accurately reflected sympathetic effector function than did normalised units or the ratio of low frequency to high frequency. Atropine did not affect high frequency heart rate variability in transplant recipients. CONCLUSIONS: The low frequency component of heart rate variability is directly related to sympathetic reinnervation to the sinus node.

Coronary Angiography↗

PubMed1977

Effects of oral amines on the EEG.

Oral tyramine activated pre-existing episodic EEG abnormalities--namely, sharp waves, spike and wave, and localised theta activity--in epileptic patients. Little change was found in the EEGs of migrainous subjects after chocolate or beta-phenylethylamine. The implications of the findings with tyramine are discussed.

Administration, Oral↗

PubMed1983

Amine content of vaginal fluid from patients with trichomoniasis and gardnerella associated non-specific vaginitis.

Amounts of putrescine, cadaverine, and tyramine were measured in vaginal washings from five patients with non-specific vaginitis (NSV) associated with Gardnerella vaginalis, five patients with trichomoniasis, and five healthy controls. Putrescine and cadaverine were present in all but one sample from the infected patients; tyramine was found in four of five samples from the women with NSV and in two of five samples from those with trichomoniasis. The mean cadaverine to putrescine ratio was significantly higher in the patients with NSV than in those with trichomoniasis. Samples from the five controls contained only very small amounts of any of the three amines. The amine content of nine of 10 samples from the infected women was reduced to normal values after metronidazole treatment. The possible sources of the amines from Trichomonas vaginalis and Gardnerella vaginalis are discussed with reference to the clinical response to treatment.

Amines↗

PubMedDate not supplied

PACAP enhances stimulation-induced norepinephrine release in canine pancreas in vivo.

The present study was to investigate whether pituitary adenylate cyclase activating polypeptide (PACAP) can modify norepinephrine (NE) release in response to pancreatic nerve stimulation in anesthetized dogs. Plasma catecholamine concentrations in aortic and superior pancreaticoduodenal (SPD) venous blood were determined by a high performance liquid chromatography method. SPD venous blood flow was measured with an electromagnetic flowmeter. Pancreatic nerves were directly stimulated for 1 min (2 ms, 12 V) at various frequencies at the level of the SPD artery. Various doses of PACAP1-27 (PACAP27) were locally infused into the pancreas through the SPD artery. Nerve stimulation significantly increased both SPD venous NE concentration and its output from the pancreas in a frequency-dependent manner. With PACAP27 alone, neither SPD venous NE concentration nor its output changed significantly following the local administration of PACAP27 at any dose tested. In the presence of PACAP27, however, the net increases in NE concentration and its output in response to nerve stimulation at 2 Hz were significantly enhanced in a dose-dependent manner. The enhanced NE responses to nerve stimulation by PACAP27 were thus significantly greater than those obtained from the group receiving either PACAP27 or stimulation alone. Increases in NE concentration and its output induced by local administration of tyramine were virtually abolished by desipramine, a neural amine uptake inhibitor. However, the NE response to tyramine was not diminished by PACAP27. The results indicate that PACAP27 enhances the stimulation-induced NE release in the pancreas, and that this facilitatory effect of PACAP27 does not result from an inhibition of the neural amine uptake mechanism. The study suggests that PACAP receptor-mediated mechanisms may be involved either directly or indirectly in the local modulation of neural NE release in the canine pancreas in vivo.

Adrenergic Uptake Inhibitors↗

PubMed1986

The noradrenaline content and innervation of brown adipose tissue in the young rabbit.

This work examined the noradrenaline content of brown adipose tissue, the metabolic response to endogenous noradrenaline released during tyramine infusion, and the innervation of brown fat at the electron microscopic level in the young rabbit. The noradrenaline content (ng/g) of the interscapular and cervical fat deposits ranged from 256 +/- 51 to 343 +/- 59 and 399 +/- 18 to 694 +/- 92, respectively, in four groups of rabbits (1-2, 7-8, 12-13, and 25-27 days of age). There was considerable variation amongst animals in each age group, but no evidence of a major increase or decrease in noradrenaline content during the first 4 weeks of life. Intravenous infusion of tyramine (100 micrograms X kg-1 X min-1) increased plasma noradrenaline concentration, oxygen consumption, and blood flow to brown fat. Thus noradrenaline released from endogenous sites, as well as injected noradrenaline, will initiate the thermogenic response of brown fat. Ultrastructurally, unmyelinated axons that were not organized in a fascicle were observed adjacent to the adipocytes in the late gestation fetus. By 1 week of age of axons were surrounded by Schwann cell cytoplasm which formed a fascicle. However, no evidence of myelination was found up to 21 days of age. Collectively, the data indicate that the brown adipocyte is fully responsive at 1-2 days of age even though myelination of the nerves is incomplete, and that the incomplete development of the sympathetic nerves at birth is not a factor in the synthesis of noradrenaline in the very young rabbit. In addition, brown fat of the newborn rabbit is not as thermogenically active as the brown fat of the cold-acclimated rat.

Adipose Tissue↗

PubMed1987

Norepinephrine storage, distribution, and release in diabetic cardiomyopathy.

The ability of hearts to store, distribute, and release norepinephrine (NE) was investigated in rats 8 wk after the induction of diabetes by an injection of streptozotocin (65 mg/kg iv). Chronic diabetes was associated with increased content and concentration of NE in heart and in other tissues such as kidney, brain, and spleen. Reserpine or tyramine treatment resulted in depletion of endogenous cardiac NE in control and diabetic rats. The depletion of NE stores at different times after a dose of reserpine was greater in diabetic hearts. On the other hand, NE stores in diabetic hearts were less sensitive than control hearts to low doses of tyramine but were more sensitive to high doses. The uptake of [3H]NE was greater in diabetic hearts in isolated perfused preparations. In comparison with the control values, diabetic hearts showed a decrease in [3H]NE in the granular fraction and an increase in the supernatant fraction. Diabetic hearts also showed an accelerated spontaneous release of [3H]NE. The increased cardiac NE and the uptake and release of NE in diabetic animals were reversible upon treatment with insulin. These results are consistent with the view that sympathetic activity is increased in diabetic cardiomyopathy and indicate that cardiac NE in diabetic rats is maintained at a higher level partly due to an increased uptake of released NE by adrenergic nerve terminals.

Animals↗

PubMed2003

Mechanisms of postspaceflight orthostatic hypotension: low alpha1-adrenergic receptor responses before flight and central autonomic dysregulation postflight.

Although all astronauts experience symptoms of orthostatic intolerance after short-duration spaceflight, only approximately 20% actually experience presyncope during upright posture on landing day. The presyncopal group is characterized by low vascular resistance before and after flight and low norepinephrine release during orthostatic stress on landing day. Our purpose was to determine the mechanisms of the differences between presyncopal and nonpresyncopal groups. We studied 23 astronauts 10 days before launch, on landing day, and 3 days after landing. We measured pressor responses to phenylephrine injections; norepinephrine release with tyramine injections; plasma volumes; resting plasma levels of chromogranin A (a marker of sympathetic nerve terminal release), endothelin, dihydroxyphenylglycol (DHPG, an intracellular metabolite of norepinephrine); and lymphocyte beta(2)-adrenergic receptors. We then measured hemodynamic and neurohumoral responses to upright tilt. Astronauts were separated into two groups according to their ability to complete 10 min of upright tilt on landing day. Compared with astronauts who were not presyncopal on landing day, presyncopal astronauts had 1). significantly smaller pressor responses to phenylephrine both before and after flight; 2). significantly smaller baseline norepinephrine, but significantly greater DHPG levels, on landing day; 3). significantly greater norepinephrine release with tyramine on landing day; and 4). significantly smaller norepinephrine release, but significantly greater epinephrine and arginine vasopressin release, with upright tilt on landing day. These data suggest that the etiology of orthostatic hypotension and presyncope after spaceflight includes low alpha(1)-adrenergic receptor responsiveness before flight and a remodeling of the central nervous system during spaceflight such that sympathetic responses to baroreceptor input become impaired.

Adrenergic alpha-Agonists↗

PubMed2001

Macrophage and type II cell catabolism of SP-A and saturated phosphatidylcholine in mouse lungs.

Type II cells and macrophages are the major cells involved in the alveolar clearance and catabolism of surfactant. We measured type II cell and macrophage contributions to the catabolism of saturated phosphatidylcholine and surfactant protein A (SP-A) in mice. We used intratracheally administered SP-A labeled with residualizing (125)I-dilactitol-tyramine, radiolabeled dipalmitoylphosphatidylcholine ([(3)H]DPPC), and its degradation-resistant analog [(14)C]DPPC-ether. At 15 min and 7, 19, 29, and 48 h after intratracheal injection, the mice were killed; alveolar lavage was then performed to recover macrophages and surfactant. Type II cells and macrophages not recovered by the lavage were subsequently isolated by enzymatic digestion of the lung. Radioactivity was measured in total lung, lavage fluid macrophages, alveolar washes, type II cells, and lung digest macrophages. Approximately equal amounts of (125)I-dilactitol-tyramine-SP-A and [(14)C]DPPC-ether associated with the macrophages (lavage fluid plus lung digest) and type II cells when corrected for the efficiency of type II cell isolation. Eighty percent of the macrophage-associated radiolabel was recovered from lung digest macrophages. We conclude that macrophages and type II cells contribute equally to saturated phosphatidylcholine and SP-A catabolism in mice.

1,2-Dipalmitoylphosphatidylcholine↗

PubMed1986

Mechanisms of adrenergic control of blood pressure in developing rats.

The rat is a species in which the sympathetic nervous system (SNS) is highly immature at birth. Blood pressure was measured directly in anesthetized preparations starting on the first postnatal day (days 1, 5, 9, 20, 40, 55, and 85), and pharmacological tests were used to evaluate the functional development of the vasomotor nerves (maximum pressor response to tyramine), the sensitivity of the vasculature to direct stimulation of alpha 1-adrenoceptors (maximum and 50% effective dose of methoxamine pressor response), and relative magnitude of the SNS contribution to resting blood pressure (hypotensive response to ganglionic blockade divided by resting blood pressure). The SNS contribution was not significant on postnatal day 1, but the relative magnitude was comparable to the adult by the end of the first postnatal week. During week 1 the vasomotor nerves were functionally immature (tyramine response was 48% of mature value on day 5), and the vasculature was supersensitive to alpha 1-adrenoceptor stimulation (154% of mature value). Conversely, in postnatal weeks 2 and 3, when the developing SNS is known to be hyperactive, the vasculature was subsensitive to noradrenergic stimulation (60-70% of adult). The net effect was to attenuate the SNS contribution to resting blood pressure during this period (55% of adult value). We conclude that there is an inverse relation between the level of tonic SNS activity and vascular sensitivity to noradrenergic stimulation in the developing rat. Supersensitivity may be critical for cardiovascular adjustments to asphyxia perinatally when the vasomotor nerves are functionally immature; subsensitivity may act homeostatically to prevent hypertension during the developmental period when SNS is hyperactive.

Animals↗

PubMed1994

Functional capacity of nicotine-sensitive canine intrinsic cardiac neurons to modify the heart.

The capacity of intrinsic cardiac efferent parasympathetic and sympathetic neurons to modify the heart was investigated in nine anesthetized open-chest dogs with adrenal glands removed from the circulation. The effects elicited by intravenously administered isoproterenol, tyramine, and nicotine on cardiac variables were examined before and after acute decentralization of the heart. Major vessels, as well as other tissues at the base of the heart, were denuded by means of an ultrasonic aspirator that removed neural elements without damaging muscles or blood vessels. The efficacy of the acute decentralization was assured by testing cardiac responses elicited by right and left stellate ganglia and cervical vagosympathetic complex stimulations after surgery. Heart rate, atrial force, and both right and left ventricular intramyocardial systolic pressures were augmented similarly by isoproterenol and tyramine before and after acute decentralization, indicating that the surgery necessary to decentralize the heart did not obtund cardiac myocyte function. Power spectral analysis of heart rate and left ventricular chamber pressure rate of change indicated an almost complete lack of variability of these indexes after, but not before, acute decentralization. Despite these changes, similar cardiac augmentation was elicited by nicotine before and after acute decentralization. Cardiac augmentation was elicited by nicotine in acutely decentralized preparations after atropine administration but not after beta-adrenergic blockade. These data indicate that the canine intrinsic cardiac nervous system contains a significant population of nicotine-sensitive adrenergic neurons that modulate the heart. Furthermore, the intrinsic cardiac nervous system does not appear to be primarily responsible for the heart rate and ventricular pressure variability found in intact hearts.

Animals↗

PubMed1981

Adrenergic neurotransmission in airways: inhibition by acetylcholine.

Superfusion techniques were used to examine the effect of acetylcholine (ACh) on the release of norepinephrine (NE) from isolated canine airways. Trachealis strips and helical strips of intrapulmonary airways were incubated with 3H-labeled NE, rinsed, and mounted in superfusion chambers. The superfusate was collected at timed intervals for estimation of total radioactivity and for column chromatographic separation of NE and its metabolites. Field electrical stimulation (2 Hz) and tyramine perfusion (3 X 10(-5) M) increased the total radioactivity of the perfusate by increasing the amount of intact 3H-labeled NE as well as the amounts of all metabolic fractions. Both extraneuronal and neuronal uptake mechanisms were important in inactivating the NE released by either stimulus. Exogenously administered ACh (10(-6)-10(-5) M) inhibited the release of NE that was caused by nerve stimulation but not that caused by tyramine perfusion. The inhibitory effect of ACh was antagonized by atropine (10(-6) M) but not by hexamethonium (5 X 10(-6) M). We conclude that ACh inhibits the exocytotic nerve-stimulated NE release by activating muscarinic receptors on adrenergic nerve varicosities.

Acetylcholine↗

PubMed1991

Independent control of mucosal and total airway blood flow during hypoxemia.

In the larger airways, the blood circulation forms a subepithelial (mucosal) and outer (peribronchial) microvascular network. This raises the possibility that blood flow in these two networks is regulated independently. We used hypoxemia as a stimulus to induce changes in tracheal mucosal blood flow normalized for systemic arterial pressure (Qtr n) measured with an inert soluble gas technique and total bronchial blood flow (Qbr) and normalized Qbr (Qbrn) measured with an electromagnetic flow probe in anesthetized sheep. Fifteen minutes of hypoxemia [PO2 40 +/- 7 (SD) Torr] decreased mean Qtr n from 1.1 +/- 0.4 to 0.8 +/- 0.4 ml.min-1.mmHg-1.10(2) (-27%; P less than 0.05; n = 7) and increased mean Qbr n from 12.1 +/- 3.2 to 17.1 +/- 5.4 ml.min-1.mmHg-1.10(2) (+41%; P less than 0.05; n = 6). The rise in Qbr correlated with cardiac output (r = 0.68; P less than 0.05). Phentolamine pretreatment (0.1 mg/kg iv) blunted the hypoxemia-related decrease of mean Qtr n (-8%; P = NS). Tyramine (2.5 mg) applied locally to the trachea decreased mean Qtr n significantly after 30 and 45 min by 31 and 19%, respectively (P less than 0.05). 6-Hydroxydopamine (0.2 mg 4 times for 1 h locally applied) prevented the hypoxemia-induced as well as local tyramine-induced decrease in mean Qtr n (0 and 0%).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed2003

Exogenous NO administration and alpha-adrenergic vasoconstriction in human limbs.

Nitric oxide (NO) is capable of blunting alpha-adrenergic vasoconstriction in contracting skeletal muscles of experimental animals (functional sympatholysis). We therefore tested the hypothesis that exogenous NO administration can blunt alpha-adrenergic vasoconstriction in resting human limbs by measuring forearm blood flow (FBF; Doppler ultrasound) and blood pressure in eight healthy males during brachial artery infusions of three alpha-adrenergic constrictors (tyramine, which evokes endogenous norepinephrine release; phenylephrine, an alpha1-agonist; and clonidine, an alpha2-agonist). To simulate exercise hyperemia, the vasoconstriction caused by the alpha-agonists was compared during adenosine-mediated (>50% NO independent) and sodium nitroprusside-mediated (SNP; NO donor) vasodilation of the forearm. Both adenosine and SNP increased FBF from approximately 35-40 to approximately 200-250 ml/min. All three alpha-adrenergic constrictor drugs caused marked reductions in FBF and calculated forearm vascular conductance (P < 0.05). The relative reductions in forearm vascular conductance caused by the alpha-adrenergic constrictors during SNP infusion were similar (tyramine, -74 +/- 3 vs. -65 +/- 2%; clonidine, -44 +/- 6 vs. -44 +/- 6%; P > 0.05) or slightly greater (phenylephrine, -47 +/- 6 vs. -33 +/- 6%; P < 0.05) compared with the responses during adenosine. In conclusion, these results indicate that exogenous NO sufficient to raise blood flow to levels simulating those seen during exercise does not blunt alpha-adrenergic vasoconstriction in the resting human forearm.

Adenosine↗

PubMed1993

Local hypothalamic adrenoceptor activation in rat: alpha 1 inhibits and alpha 2 stimulates growth hormone secretion.

We made stereotaxic microinjections of adrenoceptor agonists and the catecholamine-releasing agent, tyramine, into the preoptic anterior hypothalamic area (PO/AHA) or the medial basal hypothalamus (MBH) of unstressed rats. Growth hormone (GH) plasma concentrations were measured serially before and after intrahypothalamic injections. Noradrenaline and phenylephrine inhibited GH secretion wherever injected but were effective at lower doses in the PO/AHA. Clonidine stimulated GH secretion at both sites, at several doses in the MBH and only at one dose in the PO/AHA. Tyramine inhibited GH when injected in the PO/AHA, but not in the MBH. We conclude: (a) alpha 1 inhibition is predominant over alpha 2 stimulation of GH on or near somatostatin neurons; (b) alpha 2 stimulation predominates over alpha 1 inhibition of GH on or near GRF neurons, and (c) endogenous catecholamines in the PO/AHA have a predominantly inhibitory effect on GH secretion.

Animals↗

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