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Articoli di riviste sul tema "Noradrenaline"

Autore: Grafiati

Pubblicato: 4 giugno 2021

Ultima modifica: 25 luglio 2025

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1

Murtazina, A. R., Yu O. Nikishina, L. K. Dil’mukhametova, A. Ya Sapronova, and M. V. Ugrumov. "The role of the brain in the regulation of peripheral noradrenaline-producing organs in rats during morphogenesis." Доклады Академии наук 486, no. 6 (2019): 748–52. http://dx.doi.org/10.31857/s0869-56524866748-752.

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This work represents one part of our research project, in which we try to prove, that in the perinatal period exist a humoral regulation between noradrenaline producing organs. In this study we used a rat model that allowed blocking synthesis of noradrenalin in the brain and evaluated gene expression and protein levels of noradrenaline key synthesis enzymes such as tyrosine hydroxylase (TH) and dopamine beta-hydroxylase (DBH) in peripheral noradrenaline producing organs. As a result we showed increased gene expression of TH and DBH in adrenal glands. This data indicate that if neonatal rat bra

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2

Rudzite, Vera, Edite Jurika, Gilbert Reibnegger, Günter Weiss, Helmut Wachter, and Dietmar Fuchs. "Influence of Kynurenine, Neopterin, Noradrenaline and Pyridoxal-5-Phosphate on Cholesterol and Phospholipid Content and Phospholipid Biosynthesis in vitro." Pteridines 4, no. 3 (1993): 126–30. http://dx.doi.org/10.1515/pteridines.1993.4.3.126.

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Summary Incorporation of fatty acids into phospholipids has been investigated using samples of rat liver tissue homogenate, Krebs-Ringer-phosphate buffer (pH = 7.4) containing 0.3% albumin, fatty acid mixture and glyceroL The addition of L-kynurenine (4 nmol/g wet weight), D-eryhro-neopterin (5 and 30 pmol/g wet weight) and noradrenaline (4 nmol/g wet weight) to incubation medium induced an increase of saturated (palmitic acid) and decrease of poly-unsaturated (linoleic and arachidonic acid) fatty acids incorporation into phospholipids. The increase of saturated fatty acids incorporation into

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3

Gushcha, V. K., S. V. Lelevich, and V. M. Sheibak. "Neurotransmitter disturbances in some parts of the rat brain and their correction under chronic and intermittent alcohol intoxication." Biomeditsinskaya Khimiya 65, no. 1 (2019): 21–27. http://dx.doi.org/10.18097/pbmc20196501021.

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The pool of key neuromediators and some neurotransmitter amino acids in cerebellum, hypothalamus and midbrain of rats exposed to chronic and different variants of interrupted alcohol intoxication was investigated. The most pronounced changes were recorded in midbrain. Chronic alcohol intoxication caused an increase in the concentrations of tyrosine, dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), noradrenaline, tryptophan, serotonin, GABA and aspartate in this part of the rat brain. Interrupted alcohol intoxication with 4 days interval is accompanied by an increase in the content of tyrosine

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4

Eisenhofer, Graeme, Murray D. Esler, Ian T. Meredith, Claudia Ferrier, Gavin Lambert, and Garry Jennings. "Neuronal Re-Uptake of Noradrenaline by Sympathetic Nerves in Humans." Clinical Science 80, no. 3 (1991): 257–63. http://dx.doi.org/10.1042/cs0800257.

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1. Plasma concentrations of [3H]dihydroxyphenylglycol, the intraneuronal metabolite of noradrenaline, were examined during intravenous infusion of [3H]noradrenaline in 43 subjects, to assess the nature of its formation. Noradrenaline re-uptake by sympathetic nerves was estimated in 11 subjects from the effects of neuronal uptake blockade with desipramine on noradrenaline clearance and plasma concentrations of [3H]dihydroxyphenylglycol and endogenous dihydroxyphenylglycol. In seven subjects noradrenaline re-uptake and spillover into plasma were examined before and during mental arithmetic or ha

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5

D’Andrea, Giovanni, Massimo Leone, Gennaro Bussone, et al. "Abnormal tyrosine metabolism in chronic cluster headache." Cephalalgia 37, no. 2 (2016): 148–53. http://dx.doi.org/10.1177/0333102416640502.

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Objective Episodic cluster headache is characterized by abnormalities in tyrosine metabolism (i.e. elevated levels of dopamine, tyramine, octopamine and synephrine and low levels of noradrenalin in plasma and platelets.) It is unknown, however, if such biochemical anomalies are present and/or constitute a predisposing factor in chronic cluster headache. To test this hypothesis, we measured the levels of dopamine and noradrenaline together with those of elusive amines, such as tyramine, octopamine and synephrine, in plasma of chronic cluster patients and control individuals. Methods Plasma leve

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6

RONGEN, Gerard A., Jacques W. M. LENDERS, Paul SMITS, and John S. FLORAS. "Comparison of two indices for forearm noradrenaline release in humans." Clinical Science 99, no. 5 (2000): 363–69. http://dx.doi.org/10.1042/cs0990363.

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Although there is as yet no method which measures directly the neuronal release of noradrenaline in humans in vivo, the isotope dilution technique with [3H]noradrenaline has been applied to estimate forearm neuronal noradrenaline release into plasma. Two different equations have been developed for this purpose: one to estimate the spillover of noradrenaline into the venous effluent, and a modified formula (often referred to as the appearance rate) which may reflect more closely changes in the neuronal release of noradrenaline into the synaptic cleft, particularly during interventions that alte

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7

Lang, Chim C., Abdul R. Rahman, David J. K. Balfour, and Allan D. Struthers. "Effect of Noradrenaline on Renal Sodium and Water Handling in Euhydrated and Overhydrated Man." Clinical Science 85, no. 4 (1993): 487–94. http://dx.doi.org/10.1042/cs0850487.

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1. The renal effects of incremental doses of intravenously infused noradrenaline were evaluated in normal subjects during two different water loads, 5 ml/kg (n = 6) and 20 ml/kg (n = 9), producing conditions of euhydration and overhydration, respectively. 2. Noradrenaline infusion rates ranged from 0.015 to 0.075 μg min−1 kg−1. In the euhydrated subjects, noradrenaline caused a dose-dependent fall in urinary sodium excretion and an increase in urinary flow rate. During overhydration similar doses of noradrenaline caused a fall in urinary sodium excretion but a decrease in urinary flow rate. 3.

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8

Eisenhofer, Graeme, David S. Goldstein, and Irwin J. Kopin. "Plasma dihydroxyphenylglycol for estimation of noradrenaline neuronal re-uptake in the sympathetic nervous system in vivo." Clinical Science 76, no. 2 (1989): 171–82. http://dx.doi.org/10.1042/cs0760171.

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Abstract (sommario):

1. Neuronal re-uptake is the primary means for terminating the actions of endogenously released noradrenaline. A portion of the recaptured noradrenaline is deaminated to form dihydroxyphenylglycol. The present report describes a technique using plasma dihydroxyphenylglycol for estimation of the rate of neuronal reuptake of endogenous noradrenaline in vivo. 2. Neuronal re-uptake of noradrenaline in the sympathetic nervous system of the rat was estimated from the effects of neuronal uptake blockade with desipramine on three variables: (i) the plasma clearance of intravenously infused 3H-labelled

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9

Lamontagne, Daniel, Nobuharu Yamaguchi, Christophe Ribuot, Jacques de Champlain, and Réginald Nadeau. "Reduction of tissue noradrenaline content in the isolated perfused rat heart during ischemia: importance of monoamine oxidation." Canadian Journal of Physiology and Pharmacology 69, no. 8 (1991): 1190–95. http://dx.doi.org/10.1139/y91-174.

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The effect of ischemia on myocardial noradrenaline concentration and endogenous noradrenaline output was studied in the isolated perfused rat heart. Following a 15-min stabilization period, regional ischemia was produced by coronary artery ligation. After 60 min of ischemia, noradrenaline concentrations were significantly reduced in the interventricular septum and left ventricle but not in the right ventricle. The reduction in tissue noradrenaline concentration was not prevented when the 60-min ischemia was replaced by a 10-min ischemia followed by a 50-min perfusion. No modification in noradr

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10

Hammond, James R., Wenda F. MacDonald, and Thomas D. White. "Evoked secretion of [3H]noradrenaline and ATP from nerve varicosities isolated from the myenteric plexus of the guinea pig ileum." Canadian Journal of Physiology and Pharmacology 66, no. 3 (1988): 369–75. http://dx.doi.org/10.1139/y88-062.

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Neuronal varicosities, isolated from the myenteric plexus of guinea pig ileum longitudinal muscle, were incubated with [3H]noradrenaline to label the contents of the noradrenergic secretory vesicles. Exposure of these varicosities to KCl, nicotine, or acetylcholine resulted in the Ca2+-dependent release of [3H]noradrenaline. Veratridine also evoked a large efflux of [3H] from this preparation, but this release was only partially Ca2+ dependent. The α2-adrenoceptor agonist, clonidine, inhibited the K+-, nicotine-, and acetylcholine-induced release of [3H]noradrenaline. Similarly, exogenously ad

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11

Grønlund, Bo, Arne Astrup, Peter Bie, and Niels Juel Christensen. "Noradrenaline release in skeletal muscle and in adipose tissue studied by microdialysis." Clinical Science 80, no. 6 (1991): 595–98. http://dx.doi.org/10.1042/cs0800595.

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1. In adipose tissue and in skeletal muscle the extracellular noradrenaline levels were studied by microdialysis in the conscious dog and compared with the noradrenaline concentration in arterial plasma. 2. The experiments were performed with and without tyramine added to the perfusion medium, and noradrenaline was measured by a sensitive radioenzymic assay. 3. In the absence of tyramine, the interstitial noradrenaline levels in adipose tissue and skeletal muscles were similar to arterial blood concentrations, provided that the former were corrected for recovery. The recovery estimated from ex

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12

Fukuda, Y., M. Imoto, Y. Koyama, Y. Miyazawa, and T. Hayakawa. "Demonstration of Noradrenaline-Immunoreactive Nerve Fibres in the Liver." Journal of International Medical Research 24, no. 6 (1996): 466–72. http://dx.doi.org/10.1177/030006059602400603.

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To demonstrate noradrenaline-immunoreactive nerve fibres in liver tissues, we used an antibody to noradrenaline in the immunostaining of liver tissues from rats, guinea-pigs and humans. The tissue specimens were fixed by perfusion or immersion with cacodylate buffer containing sodium metabisulphate and glutaraldehyde, and cryostat sections were prepared. An indirect peroxidase-labelled antibody method was used for staining noradrenaline. Noradrenaline-immunoreactive nerve fibres were localized around blood vessels in the portal area and around the central vein. There were differences between t

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13

Inokuchi, Hiroe, Megumu Yoshimura, Canio Polosa та Syogoro Nishi. "Adrenergic receptors (α1 and α2) modulate different potassium conductances in sympathetic preganglionic neurons". Canadian Journal of Physiology and Pharmacology 70, S1 (1992): S92—S97. http://dx.doi.org/10.1139/y92-249.

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Intracellular recordings were made from 168 sympathetic preganglionic neurons in the slice of the second or third thoracic spinal-cord segment of the adult cat to study the actions of noradrenaline on these neurons. Noradrenaline, applied by superfusion (0.5–50 μM), produced membrane depolarization in 73 neurons and membrane hyperpolarization in 39 neurons. In 26 neurons noradrenaline produced a biphasic response (depolarization–hyperpolarization or vice versa). The depolarization was blocked by prazosin, while the hyperpolarization was blocked by yohimbine. The noradrenaline-induced depolariz

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14

SHIMIZU, Yasutake, Danuta KIELAR, Yasuhiko MINOKOSHI, and Takashi SHIMAZU. "Noradrenaline increases glucose transport into brown adipocytes in culture by a mechanism different from that of insulin." Biochemical Journal 314, no. 2 (1996): 485–90. http://dx.doi.org/10.1042/bj3140485.

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Glucose uptake into brown adipose tissue has been shown to be enhanced directly by noradrenaline (norepinephrine) released from sympathetic nerves. In this study we characterized the glucose transport system in cultured brown adipocytes, which responds to noradrenaline as well as insulin, and analysed the mechanism underlying the noradrenaline-induced increase in glucose transport. Insulin increased 2-deoxyglucose (dGlc) uptake progressively at concentrations from 10-11 to 10-6 M, with maximal stimulation at 10-7 M. Noradrenaline concentrations ranging from 10-8 to 10-6 M also enhanced dGlc up

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15

Lavoie, Julie L., François Trudeau, and Louise Béliveau. "Effect of blood flow and muscle contraction on noradrenaline spillover in the canine gracilis muscle." Canadian Journal of Physiology and Pharmacology 78, no. 1 (1999): 75–80. http://dx.doi.org/10.1139/y99-116.

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Many authors have reported that, during exercise, noradrenaline spillover increases and fractional extraction decreases. It has been suggested that the increase in blood flow to active muscles may contribute to these effects. Muscle contraction also causes changes in many factors that may affect noradrenaline spillover and fractional extraction. In this experiment, we studied the effect of muscle contraction and blood flow on noradrenaline and adrenaline spillover and fractional extraction in the in situ canine gracilis muscle. The low intensity stimulation protocol enabled us to have muscle c

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16

Chang, Peter C., Eugene Kriek, Jacques A. Van Der Krogt, Gerard-Jan Blauw, and Peter Van Brummelen. "Haemodynamic effects of physiological concentrations of circulating noradrenaline in man." Clinical Science 75, no. 5 (1988): 469–75. http://dx.doi.org/10.1042/cs0750469.

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1. To define the role of circulating noradrenaline in cardiovascular regulation, threshold concentrations for haemodynamic effects were determined in arterial and venous plasma of eight healthy volunteers. 2. Five doses of noradrenaline, 0–54 ng min−1 kg−1, were infused intravenously in random order and single-blind for 15 min per dose. Changes in intra-arterial blood pressure, heart rate, forearm blood flow and forearm vascular resistance were determined, and plasma noradrenaline was measured in arterial and venous blood samples. 3. Significant increases in systolic and diastolic blood pressu

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17

Fukuda, Y., M. Imoto, I. Nakano, Y. Katano, and T. Hayakawa. "Detection of Noradrenaline-Immunoreactive Nerve Fibres in Rat Liver by Immunoelectron Microscopy." Journal of International Medical Research 25, no. 6 (1997): 354–58. http://dx.doi.org/10.1177/030006059702500605.

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Noradrenergic innervation of rat liver was studied immunohistochemically using antibody to noradrenaline at the electron-microscopic level. Noradrenaline-immunoreactive nerve fibres were located in the portal tract and some were in close contact with the portal vein and hepatic artery. Noradrenaline-immunoreactive fibres were found to contain many vesicles that were reactive to anti-noradrenaline antibody. This preliminary study suggests that the method for detecting noradrenaline-immunoreactive fibres using the antibody is useful for studies at the electron-microscopic level.

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18

McCance, Alastair J., and J. Colin Forfar. "Cardiac and Whole-Body [3H]Noradrenaline Kinetics during Adrenaline Infusion in Man." Clinical Science 80, no. 3 (1991): 227–33. http://dx.doi.org/10.1042/cs0800227.

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1. To investigate the possible role of adrenaline as a modulator of noradrenaline release from the sympathetic nervous system, the responses of cardiac and whole-body noradrenaline kinetics to intravenous infusions of adrenaline (30 ng min−1 kg−1) and matching saline placebo were determined at rest and during supine bicycle exercise in 16 patients undergoing cardiac catheterization, in whom β-adrenoceptor antagonists had been discontinued for 72 h. 2. At rest and compared with placebo, infusion of adrenaline was associated with a small increase in arterial plasma noradrenaline from 211 ± 129 p

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19

Bacon, Travis J., Anthony E. Pickering та Jack R. Mellor. "Noradrenaline Release from Locus Coeruleus Terminals in the Hippocampus Enhances Excitation-Spike Coupling in CA1 Pyramidal Neurons Via β-Adrenoceptors". Cerebral Cortex 30, № 12 (2020): 6135–51. http://dx.doi.org/10.1093/cercor/bhaa159.

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Abstract Release of the neuromodulator noradrenaline signals salience during wakefulness, flagging novel or important experiences to reconfigure information processing and memory representations in the hippocampus. Noradrenaline is therefore expected to enhance hippocampal responses to synaptic input; however, noradrenergic agonists have been found to have mixed and sometimes contradictory effects on Schaffer collateral synapses and the resulting CA1 output. Here, we examine the effects of endogenous, optogenetically driven noradrenaline release on synaptic transmission and spike output in mou

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20

Nutt, David. "Noradrenaline revisited." Journal of Psychopharmacology 5, no. 4 (1991): 442–44. http://dx.doi.org/10.1177/026988119100500444.

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21

Post, Claes, Ewa Arweström, Bruce G. Minor, Jarl E. S. Wikberg, Gösta Jonsson, and Trevor Archer. "Noradrenaline depletion increases noradrenaline-induced antinociception in mice." Neuroscience Letters 59, no. 1 (1985): 105–9. http://dx.doi.org/10.1016/0304-3940(85)90222-8.

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22

Jana, Barbara, Jarosław Całka, Michał Bulc, and Krzysztof Witek. "Role of Noradrenaline and Adrenoreceptors in Regulating Prostaglandin E2 Synthesis Cascade in Inflamed Endometrium of Pigs." International Journal of Molecular Sciences 24, no. 6 (2023): 5856. http://dx.doi.org/10.3390/ijms24065856.

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In the inflamed uterus, the production and secretion of prostaglandins (PGs) and noradrenergic innervation pattern are changed. Receptor-based control of prostaglandin E2 (PGE2) production and secretion by noradrenaline during uterine inflammation is unknown. The aim of this study was to determine the role of α1-, α2- and β-adrenoreceptors (ARs) in noradrenaline-influenced PG-endoperoxidase synthase-2 (PTGS-2) and microsomal PTGE synthase-1 (mPTGES-1) protein levels in the inflamed pig endometrium, and in the secretion of PGE2 from this tissue. E. coli suspension (E. coli group) or saline (CON

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23

Abraham, William T., Johannes Hensen, and Robert W. Schrier. "Elevated Plasma Noradrenaline Concentrations in Patients with Low-Output Cardiac Failure: Dependence on Increased Noradrenaline Secretion Rates." Clinical Science 79, no. 5 (1990): 429–35. http://dx.doi.org/10.1042/cs0790429.

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1. Plasma noradrenaline concentrations are elevated in patients with congestive heart failure; however, the pathogenesis of these elevated noradrenaline levels is controversial. 2. Possible mechanisms for elevated noradrenaline concentrations in patients with congestive heart failure include increased noradrenaline secretion, decreased clearance of noradrenaline, and a combination of increased secretion and decreased clearance. 3. In the present study, plasma noradrenaline clearance and apparent secretion rates were determined using a whole-body steady-state radionuclide tracer method in six o

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Smith, C. C. T., B. N. C. Prichard, and D. J. Betteridge. "Plasma and platelet free catecholamine concentrations in patients with familial hypercholesterolaemia." Clinical Science 82, no. 1 (1992): 113–16. http://dx.doi.org/10.1042/cs0820113.

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1. Plasma and platelet free catecholamine concentrations were measured in 22 normal subjects and in 10 treated and 11 untreated patients with heterozygous familial hypercholesterolaemia. 2. Plasma noradrenaline concentrations were significantly higher in both treated and untreated hypercholesterolaemic patients than in normal subjects. Adrenaline concentrations did not differ. 3. Platelet noradrenaline levels were higher in untreated hypercholesterolaemic patients than in normal subjects. 4. Positive correlations between the plasma noradrenaline concentration and the platelet noradrenaline con

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25

Cañas, N., D. Sanchis, G. Gómez, et al. "3-Hydroxybutyrate co-infused with noradrenaline decreases resulting plasma levels of noradrenaline in Wistar rats." Journal of Experimental Biology 200, no. 20 (1997): 2641–46. http://dx.doi.org/10.1242/jeb.200.20.2641.

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Pentobarbital-anaesthetized male Wistar rats were infused with 6microgkg-1min-1 of noradrenaline. The infusion was supplemented with 8.5 mgkg-1min-1 of D-3-hydroxybutyrate (3-OHB) for 15 min in order to determine its effect on the adrenergic response of the rat. Plasma levels of noradrenaline rose to a plateau of approximately 50 nmoll-1 with infusion. In the group infused with noradrenaline alone, noradrenaline levels were maintained for 1h. Supplementation with 3-OHB induced a decrease in plasma noradrenaline level that was inversely correlated with 3-OHB level. Aortic and interscapular brow

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26

Thoroed, S., M. Soergaard, E. Cragoe, and K. Fugelli. "The osmolality-sensitive taurine channel in flounder erythrocytes is strongly stimulated by noradrenaline under hypo-osmotic conditions." Journal of Experimental Biology 198, no. 2 (1995): 311–24. http://dx.doi.org/10.1242/jeb.198.2.311.

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Stimulation of flounder erythrocytes by noradrenaline under isosmotic conditions (330 mosmol kg-1) and physiological Na+ concentration (113 mmol l-1) caused swelling of the cells. The EC50 of this cell swelling was 0.65 &micro;mol l-1 noradrenaline. The effect of the noradrenaline-induced cell swelling on the taurine channel under isosmotic conditions was negligible. However, when the cells were stimulated by noradrenaline (1.0 &micro;mol l-1) before, simultaneously with or after reduction of osmolality (255 mosmol kg-1), the volume regulatory efflux of taurine mediated by the taurine

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Abebe, Worku, Kim Howard Harris, and Kathleen M. MacLeod. "Role of extracellular Ca2+ in the selective enhancement of contractile responses of arteries from diabetic rats to noradrenaline." Canadian Journal of Physiology and Pharmacology 72, no. 12 (1994): 1544–51. http://dx.doi.org/10.1139/y94-222.

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Maximum contractile responses of diabetic aortas incubated in the absence of extracellular Ca2+ to increasing Ca2+ (0.01–10 mM) in the presence of 1 μM noradrenaline, but not 40 mM KCl, were significantly increased compared with those of age-matched control rats. Maximum contractile responses of both aortas and mesenteric arteries from diabetic rats to noradrenaline, but not KCl, in the presence of extracellular Ca2+ (2.5 mM) were also significantly enhanced. The Ca2+ channel antagonists verapamil and nifedipine and the Ca2+ channel agonist BAY K8644 produced a similar percentage change in the

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Morgan, N. G., and W. Montague. "Studies on the mechanism of inhibition of glucose-stimulated insulin secretion by noradrenaline in rat islets of Langerhans." Biochemical Journal 226, no. 2 (1985): 571–76. http://dx.doi.org/10.1042/bj2260571.

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Noradrenaline (norepinephrine) was shown to be a potent inhibitor of glucose-induced insulin release from rat pancreatic islets, with half-maximal inhibition of the secretory response to 20 mM-glucose occurring at approx. 0.3 microM, and complete suppression of the response occurring at 4 microM-noradrenaline. Inhibition of insulin secretion by noradrenaline was antagonized by the alpha 2-adrenergic antagonist yohimbine (half maximally effective dose approximately 1 microM), but was largely unaffected by the alpha 1-adrenergic antagonist prazosin at concentrations up to 50 microM, suggesting t

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Howes, L. G., and J. L. Reid. "Changes in plasma free 3,4-dihydroxyphenylethylene glycol and noradrenaline levels after acute alcohol administration." Clinical Science 69, no. 4 (1985): 423–28. http://dx.doi.org/10.1042/cs0690423.

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1. The effects of alcohol (0.9 g/kg) compared with placebo (400 ml of orange juice) on plasma noradrenaline and 3,4-dihydroxyphenylethylene glycol levels, and on erect and supine blood pressures and heart rates, were studied in eight normal male volunteers. 2. Alcohol caused a rise in noradrenaline levels that commenced approximately 30 min after drinking and lasted about 4h. In contrast, 3,4-dihydroxyphenylethylene glycol levels fell immediately after alcohol administration and remained low for at least 6h. Acute alcohol administration alters noradrenaline catabolism, and may have a dual effe

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Smith, C. C. T., A. P. Wilson, B. N. C. Prichard, and D. J. Betteridge. "Platelet efflux of noradrenaline in patients with type 1 diabetes mellitus." Clinical Science 76, no. 6 (1989): 603–7. http://dx.doi.org/10.1042/cs0760603.

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1. Endogenous noradrenaline release from washed platelets incubated under resting conditions and in the presence of thrombin was examined in 14 normal subjects and 10 subjects with type 1 (insulin-dependent) diabetes. 2. Irreversible aggregation of platelets from both normal and diabetic subjects was induced by thrombin (0.3 unit/ml). Platelets from diabetic subjects were more sensitive than platelets from normal subjects, extents of aggregation being 89% and 76%, respectively (P < 0.002). 3. Stimulation with thrombin (0.3 unit/ml) elicited marked platelet release of noradrenaline to the in

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Quintas, Clara, Jorge Gonçalves, and Glória Queiroz. "Involvement of P2Y1, P2Y6, A1 and A2A Receptors in the Purinergic Inhibition of NMDA-Evoked Noradrenaline Release in the Rat Brain Cortex." Cells 12, no. 13 (2023): 1690. http://dx.doi.org/10.3390/cells12131690.

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In the cerebral cortex, glutamate activates NMDA receptors (NMDARs), localized in noradrenergic neurons, inducing noradrenaline release that may have a permissive effect on glutamatergic transmission, and therefore, on the modulation of long-term plasticity. ATP is co-released with noradrenaline, and with its metabolites (ADP and adenosine) is involved in the purinergic modulation of electrically-evoked noradrenaline release. However, it is not known if noradrenaline release evoked by activation of NMDARs is also under purinergic modulation. The present study aimed to investigate and to charac

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Lavoie, Julie L., and Louise Béliveau. "Bradykinin facilitates noradrenaline spillover during contraction in the canine gracilis muscle." Canadian Journal of Physiology and Pharmacology 79, no. 10 (2001): 831–35. http://dx.doi.org/10.1139/y01-062.

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Noradrenaline spillover from skeletal muscle vascular areas increases during exercise but the underlying mechanisms are not well understood. Muscle contraction itself causes changes in many factors that could affect noradrenaline spillover. For instance, it has been reported that bradykinin is synthesized in skeletal muscle areas during contraction. Because the B2 bradykinin receptor facilitates noradrenaline spillover, it may be involved in the increase associated with contraction. In this experiment, we studied the effect of bradykinin on noradrenaline spillover in the in situ canine gracili

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Woodward, J. A., and E. D. Saggerson. "Effect of adenosine deaminase, N6-phenylisopropyladenosine and hypothyroidism on the responsiveness of rat brown adipocytes to noradrenaline." Biochemical Journal 238, no. 2 (1986): 395–403. http://dx.doi.org/10.1042/bj2380395.

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Abstract (sommario):

Adenosine deaminase (1 unit/ml) potentiated the lipolytic action of noradrenaline in adipocytes isolated from brown adipose tissue of 1- and 6-week-old rats by decreasing the EC50 (concn. giving 50% of maximal effect) for noradrenaline by 3-4-fold. With cells from neonatal rabbit tissue, adenosine deaminase only had a small, non-significant, effect on the EC50 for noradrenaline. Lipolysis in rat brown adipocytes was inhibited by low concentrations of N6-phenylisopropyladenosine (PIA). Rabbit cells were far less sensitive to PIA. PIA, prostaglandin E1 and nicotinate all inhibited noradrenaline-

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34

Thompson, Jane M., B. Gunnar Wallin, Gavin W. Lambert, Garry L. Jennings, and Murray D. Esler. "Human Muscle Sympathetic Activity and Cardiac Catecholamine Spillover: No Support for Augmented Sympathetic Noradrenaline Release by Adrenaline Co-Transmission." Clinical Science 94, no. 4 (1998): 383–93. http://dx.doi.org/10.1042/cs0940383.

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Abstract (sommario):

1. Evidence from animal studies indicates that circulating adrenaline may be taken up into sympathetic nerves, facilitating the release of noradrenaline. To test whether adrenaline acts as a co-transmitter in humans we studied eight healthy men (aged 19–23 years) during isometric handgrip before and after an adrenaline infusion (1–3 μg/min for > 30 rain). Sympathetic activity was assessed using radiotracer kinetic techniques to measure total and cardiac spillovers of noradrenaline and adrenaline, and microneurography to measure muscle sympathetic activity. 2. During the adrenaline infusion

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35

Knudsen, J. H., F. Gustafsson, J. Toft, and N. J. Christensen. "Lymphocyte cAMP and Ageing: Significance of Subset Composition, Plasma Noradrenaline, Regular Physical Training and Long-Term Smoking." Clinical Science 91, no. 5 (1996): 621–26. http://dx.doi.org/10.1042/cs0910621.

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Abstract (sommario):

1. We studied 37 healthy men at rest in the supine position to examine the effect of ageing, smoking and physical training on β2-adrenoceptor function, plasma catecholamines and the proportions of various lymphocyte subsets. 2. In 14 young subjects the proportion of natural killer cells was correlated with cAMP production in lymphocytes and inversely correlated with plasma noradrenaline level. 3. In 16 elderly non-smokers plasma noradrenaline was negatively correlated with the natural killer cell subset CD3–CD16+. Lymphocyte cAMP responses did not differ between young and elderly non-smokers,

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36

SØNDERGAARD, Susanne B., Jens H. KNUDSEN, and Niels J. CHRISTENSEN. "Regulation of cAMP in a lymphocyte preparation isolated from peripheral venous blood in human subjects: the significance of residual thrombocytes, noradrenaline and prostaglandins." Clinical Science 95, no. 3 (1998): 377–83. http://dx.doi.org/10.1042/cs0950377.

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Abstract (sommario):

1.The aim of the study was to elucidate the mechanism of the previously reported close correlation observed between noradrenaline and cAMP in a lymphocyte preparation (LP) isolated from peripheral venous blood in healthy subjects. A close correlation was also obtained in the present study between lymphocyte noradrenaline and adrenaline and cAMP both in the basal state and after stimulation with isoproterenol (P< 0.05 to 0.007). 2.Although 99% of the thrombocytes were removed from the LP during the washing procedure, LP contained approximately one thrombocyte per lymphocyte. The noradrenalin

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37

Maes, M., M. Vandewoude, C. Schotte, M. Martin, and P. Blockx. "Positive relationship between the catecholaminergic turnover and the DST results in depression." Psychological Medicine 20, no. 3 (1990): 493–99. http://dx.doi.org/10.1017/s0033291700017001.

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Abstract (sommario):

SynopsisIn the past some workers have reported positive relationships between indices of noradrenaline activity and measures of hypothalamic–pituitary–adrenal (HPA)-axis function. In order to investigate these relations, the authors measured noradrenaline, adrenaline and vanillylmandelic acid (VMA) in 24 h urine samples of 72 depressed females. Serum adrenocorticotrophic hormone (ACTH) and cortisol concentrations were determined before and after administration of 1 mg of dexamethasone. Cortisol non-suppressors exhibited a significantly higher noradrenaline, adrenaline and VMA excretion as comp

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38

Popp-Snijders, C., B. Geenen, and E. A. P. Van Der Heijden. "Serum Noradrenaline is Composed of Plasma and Platelet Noradrenaline." Annals of Clinical Biochemistry: International Journal of Laboratory Medicine 26, no. 2 (1989): 191–92. http://dx.doi.org/10.1177/000456328902600219.

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39

Smith, C. C. T., L. D. Curtis, A. P. Delamothe, B. N. C. Prichard, and D. J. Betteridge. "The Distribution of Catecholamines between Platelets and Plasma in Normal Human Subjects." Clinical Science 69, no. 1 (1985): 1–6. http://dx.doi.org/10.1042/cs0690001.

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Abstract (sommario):

1. We have used high-performance liquid chromatography with electrochemical detection to measure content of adrenaline and noradrenaline in platelets in 13 normal subjects at rest. 2. Subjects were exercised to raise plasma catecholamine levels and promote the platelet release reaction. 3. There was a significant positive correlation between plasma noradrenaline concentrations and platelet noradrenaline content. 4. Platelet/plasma concentration ratios were 1855 for noradrenaline and 268 for adrenaline at rest and 473 and 152 respectively after exercise. 5. Plasma noradrenaline levels positivel

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40

Kelly, C. B., and S. J. Cooper. "Plasma noradrenaline response to electroconvulsive therapy in depressive illness." British Journal of Psychiatry 171, no. 2 (1997): 182–86. http://dx.doi.org/10.1192/bjp.171.2.182.

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Abstract (sommario):

BackgroundAbnormalities of catecholaminergic function have been hypothesised to cause depressive illness. Plasma noradrenaline can be used as a marker of central noradrenergic activity. It is of interest to examine the change in resting plasma noradrenaline in patients with depressive illness over a course of electroconvulsive therapy (ECT) and relate this to their clinical state.MethodPatients referred for ECT who suffered from DSM – III – R major depressive disorder or dysthymia were recruited. Blood samples were taken before and after each treatment, during a course of ECT, to measure plasm

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41

von KÄNEL, Roland, Brigitte M. KUDIELKA, Adham ABD-el-RAZIK, Marie-Louise GANDER, Karl FREY, and Joachim E. FISCHER. "Relationship between overnight neuroendocrine activity and morning haemostasis in working men." Clinical Science 107, no. 1 (2004): 89–95. http://dx.doi.org/10.1042/cs20030355.

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Abstract (sommario):

Sustained effects of SNS (sympathetic nervous system) and HPAA (hypothalamic–pituitary–adrenal axis) hyperactivity on haemostasis have not been investigated. In the present study, we tested for an association of overnight urinary catecholamine and cortisol excretion with morning plasma levels of fibrinogen, PAI-1 (plasminogen activator inhibitor-1) and D-dimer. Participants (639 male industrial employees) with a complete dataset were studied (age, 41±11 years; mean±S.D.). Subjects collected overnight urinary samples and had a fasting morning blood sample drawn. Measurement of urinary adrenalin

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42

Lee, DongJin R., Natalie J. Galant, Donghoon M. Lee, et al. "Theoretical investigation of the conformational intricacies and thermodynamic functions of noradrenaline." Canadian Journal of Chemistry 89, no. 8 (2011): 1010–20. http://dx.doi.org/10.1139/v11-076.

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Abstract (sommario):

Noradrenaline is a neurotransmitter that is involved in various psychological processes. In the neurotransmission process, noradrenaline binds to an adrenergic receptor by forming a complex of hydrogen bonds between its two catechol ring hydroxyl groups and the amino acid residues of adrenergic receptors. Although the two catechol ring hydroxyl groups play a crucial role in making hydrogen bonds to the binding site of the adrenergic receptor, the contribution of the catechol ring hydroxyl groups to the intramolecular stability that may affect docking has not been fully studied. To reveal the s

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43

Tetens, V., G. Lykkeboe, and N. J. Christensen. "Potency of adrenaline and noradrenaline for beta-adrenergic proton extrusion from red cells of rainbow trout, Salmo gairdneri." Journal of Experimental Biology 134, no. 1 (1988): 267–80. http://dx.doi.org/10.1242/jeb.134.1.267.

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Abstract (sommario):

The red cell adrenoceptor affinity for the unspecific agonists adrenaline and noradrenaline and the specific beta-agonist isoprenaline was studied in vitro on whole blood of rainbow trout, Salmo gairdneri at 15 degrees C. The erythrocytic adrenoceptors could be pharmacologically characterized as beta-receptors of the ‘noradrenaline’-type (beta 1-type), with an order of potency of isoprenaline greater than noradrenaline much greater than adrenaline. The adrenoceptor affinities, expressed as agonist concentrations for 50% response (EC50), were 1.3 X 10(−8) and 7.6 X 10(−7) mol l-1 for noradrenal

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44

Jana, Barbara, Jarosław Całka, Aneta Andronowska, Aleksandra Mówińska, Krzysztof Witek, and Katarzyna Palus. "Noradrenaline and Adrenoreceptors Are Involved in the Regulation of Prostaglandin I2 Production in the Porcine Endometrium after Experimentally Induced Inflammation." International Journal of Molecular Sciences 25, no. 12 (2024): 6313. http://dx.doi.org/10.3390/ijms25126313.

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Abstract (sommario):

Endometritis is a common disease in animals, leading to disruption of reproductive processes and economic losses. Noradrenergic control of prostaglandin (PG)I2 formation by inflamed endometrium is unknown. We determined the involvement of α1-, α2- and β-adrenoreceptors (ARs) in noradrenaline-influenced PGI synthase (PGIS) protein abundance and PGI2 release from porcine (1) endometrial explants with Escherichia coli (E. coli)-induced inflammation in vivo, and (2) E. coli lipopolysaccharide (LPS)-treated endometrial epithelial cells. Experiment 1. E. coli suspension (E. coli group) or saline (CO

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45

Jacobs, Marie-Cecile, David S. Goldstein, Jacques J. Willemsen, Paul Smits, Theo Thien, and Jacques W. M. Lenders. "Differential Effects of Low- and High-Intensity Lower Body Negative Pressure on Noradrenaline and Adrenaline Kinetics in Humans." Clinical Science 90, no. 5 (1996): 337–43. http://dx.doi.org/10.1042/cs0900337.

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Abstract (sommario):

1. Lower body negative pressure provides a means to examine neurocirculatory reflexive responses to decreases in venous return to the heart. We assessed whether the pattern of catecholaminergic responses to lower body negative pressure depends on the intensity of the stimulus (−15 versus −40 mmHg). 2. In 14 healthy subjects, responses of forearm blood flow and noradrenaline spillover and of total body noradrenaline and adrenaline spillover were assessed during infusion of [3H]noradrenaline and [3H]adrenaline during −15 and −40 mmHg of lower body negxative pressure. 3. During lower body negativ

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46

Puerta, M., M. Abelenda, M. P. Nava, and A. Fernandez. "Reduced noradrenaline responsiveness of brown adipocytes isolated from estradiol-treated rats." Canadian Journal of Physiology and Pharmacology 71, no. 10-11 (1993): 858–61. http://dx.doi.org/10.1139/y93-129.

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Abstract (sommario):

High plasma levels of estradiol are known to reduce the GDP binding of brown adipose tissue. Since GDP binding depends on the level of sympathetic discharge to brown adipose tissue, we measured the responsiveness to noradrenaline of brown adipocytes isolated from female rats with high plasma levels of estradiol. Noradrenaline responsiveness was assessed by measuring the respiration rate of isolated brown adipocytes in the presence of different concentrations of noradrenaline. Both control and treated adipocytes showed the same basal respiratory rate (27 ± 6 and 24 ± 4 nmol O2∙min−1∙10−6 cells,

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47

Hurst, R. D., and N. G. Morgan. "Evidence for differential effects of noradrenaline and somatostatin on intracellular messenger systems in rat islets of Langerhans." Journal of Molecular Endocrinology 4, no. 3 (1990): 231–37. http://dx.doi.org/10.1677/jme.0.0040231.

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Abstract (sommario):

ABSTRACT The mechanisms involved in inhibition of insulin secretion by somatostatin and noradrenaline were compared in order to establish whether the receptors for these agents are coupled to similar effector systems in the pancreatic B cell. Both agents significantly reduced forskolin-induced adenylate cyclase activity in islet homogenates, although noradrenaline was more effective than somatostatin. The capacity of noradrenaline to inhibit insulin secretion was largely unaffected by agents that increase intracellular cyclic AMP, whereas the effect of somatostatin as an inhibitor was markedly

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48

Oda, Y., K. Mashita, M. Mori-Tanaka, et al. "The inhibitory effect of noradrenaline on thyrotrophin-stimulated 3,5,3′-tri-iodothyronine and thyroxine release is mediated through a Ca2+-dependent process in the thyroid gland of the mouse." Journal of Endocrinology 138, no. 1 (1993): 73–80. http://dx.doi.org/10.1677/joe.0.1380073.

Testo completo

Abstract (sommario):

ABSTRACT We examined the effect of noradrenaline on the release of 3,5,3′-tri-iodothyronine (T3) and thyroxine (T4) from perifused mouse thyroid. Noradrenaline suppressed the thyrotrophin (TSH)-stimulated release of T3 and T4. The addition of prazosin, which is a specific α1 antagonist, or the depletion of Ca2+ from the perifusion buffer completely abolished the inhibitory effect of noradrenaline on TSH-stimulated T3 and T4 release. Noradrenaline did not inhibit TSH-stimulated cyclic adenosine 3′,5′-monophosphate (cAMP) release in the presence of 3-isobutyl-1-methylxanthine (IBMX), which inhib

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49

Pennefather, JN, JD Paull, ME Story, and SP Ziccone. "Supersensitivity to the stimulant action of noradrenaline on human myometrium near term." Reproduction, Fertility and Development 5, no. 1 (1993): 39. http://dx.doi.org/10.1071/rd9930039.

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Abstract (sommario):

Noradrenaline (10-50 nM) and tyramine (0.05-1 mM) enhanced contractile force elicited by field stimulation of strips of myometrium from non-pregnant and pregnant women. In higher concentrations, noradrenaline produced sustained contractions. The EC50 values for noradrenaline were 0.4 microM in tissues from pregnant women and 3.1 microM in tissues from non-pregnant women; maximum responses were greater in the former tissues. In addition, the effects of noradrenaline on myometrium from pregnant women were more marked on the inner layer than on the outer layer, antagonized by the alpha 1-adrenoce

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50

Baht, H. S., and E. D. Saggerson. "Effect of noradrenaline on triacylglycerol synthesis in rat brown adipocytes." Biochemical Journal 258, no. 2 (1989): 369–73. http://dx.doi.org/10.1042/bj2580369.

Testo completo

Abstract (sommario):

Incubation of rat brown adipocytes with noradrenaline in the presence of insulin and palmitate caused a decrease in the rate of triacylglycerol synthesis as measured by [U-14C]glucose incorporation into acylglycerol glycerol. Concomitantly, the ratio of [1-14C]palmitate oxidized to CO2 to that esterified was increased. This alteration in the rate of triacylglycerol synthesis by noradrenaline was not observed when fatty acid oxidation was inhibited by etomoxir. Noradrenaline did not cause any acute inactivation of enzymes of the triacylglycerol-synthesis pathway. It is suggested that the decrea

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