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Добірка наукової літератури з теми "Noradrenaline"

Автор: Grafiati

Опубліковано: 4 червня 2021

Оновлено: 31 липня 2024

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Статті в журналах з теми "Noradrenaline"

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 (June 28, 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 brain lacks an ability to produce noradrenaline, then as a compensatory process synthesis of noradrenaline increased in adrenal glands, so that the concentration levels in blood are kept at normal levels. This indicates that there is a humoral regulation between brain and adrenal glands which is not fully understood yet.

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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 (August 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 phospholipids was more pronounced after addition of neopterin and noradrenaline to the incubation medium while the decrease of linoleic and arachidonic acid synthesis was stimulated most with kynurenine. Moreover, kynurenine stimulated whereas neopterin depressed the oleic acid incorporation into phospholipids. These changes of fatty acid incorporation into phospholipids were followed by increase of cholesterol content in samples containing kynurenine, neopterin or noradrenalin. In contrast, phospholipid content decreased in samples containing kynurenine or noradrenalin, hut was not altered by supplementation of neopterin. Since the addition of kynurenine and neopterin to incubation medium for isolated fog heart resulted in an increased noradrenaline and decreased pyridoxal-5-phosphate content in the tissue, we also added pyridoxal-5-phosphate (4 nmol/g wet weight) to incubation medium for phospholipid biosynthesis. No change of the fatty acid incorporation into phospholipids as welI as the content of phospholipids and cholesterol in samples was observed.

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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 (January 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, and noradrenaline. Interrupted alcohol intoxication with 1 day interval leaded to an increase in the concentrations of tyrosine, DOPAC, noradrenalin, tryptophan, GABA, glycine and aspartate. The amino acids composition “Titacin” had a pronounced normalizing effect in the midbrain under interrupted alcohol intoxication with 1 day interval.

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4

D’Andrea, Giovanni, Massimo Leone, Gennaro Bussone, Paola Di Fiore, Andrea Bolner, Marco Aguggia, Maria Gabriella Saracco, et al. "Abnormal tyrosine metabolism in chronic cluster headache." Cephalalgia 37, no. 2 (September 30, 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 levels of dopamine, noradrenaline and trace amines, including tyramine, octopamine and synephrine, were measured in a group of 23 chronic cluster headache patients (10 chronic cluster ab initio and 13 transformed from episodic cluster), and 16 control participants. Results The plasma levels of dopamine, noradrenaline and tyramine were several times higher in chronic cluster headache patients compared with controls. The levels of octopamine and synephrine were significantly lower in plasma of these patients with respect to control individuals. Conclusions These results suggest that anomalies in tyrosine metabolism play a role in the pathogenesis of chronic cluster headache and constitute a predisposing factor for the transformation of the episodic into a chronic form of this primary headache.

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5

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 (March 1, 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 handgrip exercise. 2. During infusion of [3H]noradrenaline, plasma [3H]dihydroxyphenylglycol increased progressively, indicating its formation from previously stored [3H]noradrenaline leaking from vesicles as well as from [3H]noradrenaline metabolism immediately after removal into sympathetic nerves. Thus, to estimate noradrenaline reuptake, the amount of [3H]dihydroxyphenylglycol derived from [3H]noradrenaline metabolized immediately after removal into the sympathetic axoplasm must be isolated from that derived from [3H]noradrenaline sequestered into vesicles. 3. At rest in the supine position the rate of noradrenaline re-uptake was 474 ± 122 pmol min−1 kg−1, 9.5-fold higher than the rate of spillover of noradrenaline into plasma (49.6 ± 6.4 pmol min−1 kg−1). Noradrenaline reuptake and spillover into plasma were both increased during mental arithmetic and isometric handgrip exercise.

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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 (October 3, 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 alter forearm blood flow. The present study was performed to compare the effects of two interventions known to exert contrasting actions on neuronal forearm noradrenaline release and forearm blood flow. Intra-arterial infusion of sodium nitroprusside at doses without systemic effect increases forearm blood flow, but not neuronal noradrenaline release. In contrast, lower-body negative pressure at -25 mmHg causes forearm vasoconstriction by stimulating neuronal noradrenaline release. During sodium nitroprusside infusion, forearm noradrenaline spillover increased from 1.1±0.3 to 2.2±1.0 pmol·min-1·100 ml-1 (P < 0.05), whereas the forearm noradrenaline appearance rate was unchanged. Lower-body negative pressure did not affect the forearm noradrenaline spillover rate, but increased the forearm noradrenaline appearance rate from 3.4±0.4 pmol·min-1·100 ml-1 at baseline to 5.0±0.9 pmol·min-1·100 ml-1 (P < 0.05). These results indicate that the noradrenaline appearance rate provides the better approximation of changes in forearm neuronal noradrenaline release in response to stimuli which alter local blood flow.

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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 (October 1, 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. Although there was no detectable change in glomerular filtration rate, a dose-dependent fall in effective renal plasma flow was observed in both hydration states during noradrenaline infusion. 4. Noradrenaline infusion was associated with a dose-dependent increase in proximal tubular sodium reabsorption as assessed by the lithium clearance method. Fractional reabsorption of sodium by the distal nephron was, however, unchanged by noradrenaline in both hydration states. 5. Plasma vasopressin concentration was unchanged by noradrenaline in euhydrated subjects. The renin-angiotensin-aldosterone axis was stimulated by noradrenaline in both euhydrated and overhydrated subjects. 6. Thus we conclude that plasma circulating noradrenaline has a dose-dependent antinatriuretic effect in man. The antinatriuretic effect of noradrenaline is mediated mainly at the proximal tubule in man. We have also shown that during overhydration, noradrenaline decreased urinary flow rate. In contrast, in euhydrated subjects, noradrenaline increased urinary flow rate with no accompanying changes in plasma vasopressin concentration, which suggests a direct effect of noradrenaline on the renal tubular permeability to water.

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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 (February 1, 1989): 171–82. http://dx.doi.org/10.1042/cs0760171.

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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 noradrenaline, (ii) the plasma concentration of endogenous dihydroxyphenylglycol, and (iii) the plasma concentration of 3H-labelled dihydroxyphenylglycol formed from infused 3H-labelled noradrenaline. 3. Desipramine decreased plasma dihydroxyphenylglycol by 36%, this representing the fraction of dihydroxyphenylglycol in plasma that was derived from recaptured noradrenaline. After desipramine, the decrease in the rate of neuronal uptake of 3H-labelled noradrenaline was 9.7 times that of the decrease in the plasma spillover of 3H-labelled dihydroxyphenylglycol. Since the appearances in plasma of dihydroxyphenylglycol from unlabelled and 3H-labelled noradrenaline were similar, the neuronal re-uptake of endogenous noradrenaline could be assumed to be 9.7 times as much as the plasma spillover of dihydroxyphenylglycol that was derived from recaptured noradrenaline (0.15 nmol min−1 kg−1). 4. The rate of neuronal re-uptake of endogenous noradrenaline was estimated to be 1.45 nmol min−1 kg−1, whereas the plasma spillover of noradrenaline was 0.127 nmol min−1 kg−1. Thus, only a small fraction (<9%) of the noradrenaline released into the synaptic cleft spills over into the circulation.

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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 (August 1, 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 noradrenaline output was observed during a 60-min ischemia. In contrast, reperfusion was accompanied by a washout of noradrenaline in the coronary effluent, corresponding to only 2% of the amount lost by the tissue. The effect of monoamine oxidase inhibition during the whole ischemic period was studied by perfusing the preparation with pargyline starting 10 min before the artery ligation. Although the administration of pargyline did not alter the noradrenaline output, it did prevent a reduction in myocardial noradrenaline concentration. It was concluded that monoamine oxidase may contribute to the elimination of the noradrenaline lost by the cardiac tissue during ischemia.Key words: tissue noradrenaline, myocardial ischemia, monoamine oxidase, isolated rat heart.

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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 (March 1, 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 administered (−)noradrenaline was an effective inhibitor of the K+-evoked release of [3H]noradrenaline. The α2-adrenoceptor antagonist, yohimbine, antagonized the inhibitory actions of both clonidine and (−)noradrenaline on the K+-evoked release of [3H]noradrenaline from myenteric varicosities. Nicotine, acetylcholine, KCl, and veratridine also released ATP from these guinea pig ileal myenteric varicosities. However, the evoked release of ATP was unaffected by clonidine. These results indicate that myenteric varicosities can take up and release [3H]noradrenaline and that they possess presynaptic α2-adrenoceptors which, when activated, inhibit the release of [3H]noradrenaline. These receptors may play a role in modulating the release of noradrenaline in the myenteric plexus in vivo. In addition, the present results suggest that ATP and [3H]noradrenaline may not be released from the same population of secretory vesicles in neuronal varicosities isolated from guinea pig ileum longitudinal muscle.

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Дисертації з теми "Noradrenaline"

1

Smith, Nigel. "Plasma protein binding of noradrenaline." Thesis, University of Nottingham, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252951.

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2

Scriven, Anthony James Ivor. "Plasma noradrenaline and cardiovascular sympathetic activity." Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46541.

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3

Haywood, S. A. "GnRH network : noradrenaline and sex steroids." Thesis, University of Cambridge, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.603906.

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The first studies in this thesis use in situ hybridisation to investigate if temporal changes occur in cellular GnRH gene expression during the preovulatory phase of the oestrous cycle and further investigation gene expression in other neurotransmitter systems in the GnRH network within the preoptic area and the brainstem. It is evident from these studies that, during the oestrous cycle, transcriptional changes within GnRH, enkphalin, nitric oxide synthase and noradrenaline containing neural populations, in the preoptic area and brainstem respectively, are small, and are perhaps not pertinent to the imminent LH surge. Nevertheless, it is already established that sex steroid dependent changes in GnRH secretion are associated with an increased in noradrenergic activity. The second study, using immunocytochemical techniques, focuses on this relationship and demonstrates, for the first time, the presence of progesterone receptors (PR) in up to 35% of noradrenaline cells in caudal regions of the nucleus tractus solitarii (A2 cell group). Moreover, this study shows that dynamic fluctuations in sex steroid receptors occur during the oestrous cycle, with the highest percentage of A2 neurones expressing PR and oestrogen receptor (ERα) on proestrous morning with a nadir on dioestrous afternoon. Further studies in steroid-primed female rats provide evidence that this is predominantly an oestrogen-inducing effect on PR expression. Finally, using retrograde tracing techniques combined with dual-labelling immunocytochemistry I show that approximately 5-12% of A cells in the brainstem project to the vicinity of the GnRH perikarya located in the rostral preoptic area (rPOA) and that the majority of these projecting A2 neurones express PR.

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4

Field, Brent A. "The effects of noradrenaline on cortical signal processing /." view abstract or download file of text, 2000. http://wwwlib.umi.com/cr/uoregon/fullcit?p9978587.

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Thesis (Ph. D.)--University of Oregon, 2000.
Typescript. Includes vita and abstract. Includes bibliographical references (leaves 140-159). Also available for download via the World Wide Web; free to University of Oregon users.

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5

Kelly, Christopher Brendan. "Noradrenergic function in anxiety and depressive states." Thesis, Queen's University Belfast, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.261770.

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6

Roberts, Veronica J. "Corticosterone modulation of noradrenaline stimulated cyclic AMP formation in hippocampus." Thesis, University of Ottawa (Canada), 1985. http://hdl.handle.net/10393/4949.

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7

Brice, Carolyn F. "Caffeine : consumption, behavioural effects and the role of central noradrenaline." Thesis, University of Bristol, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.302061.

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8

Popovik, Elvira. "The role of noradrenaline in the development of rat neocortex." Thesis, University of Bristol, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289632.

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9

DONG, WEN-XIN. "Metabolisme pre-synaptique peripherique de la noradrenaline chez le rat." Paris 6, 1997. http://www.theses.fr/1997PA066067.

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Nous avons etudie le metabolisme pre-synaptique de la noradrenaline (na) chez l'animal entier ; cette voie metabolique etant la voie la plus importante pour la na synaptique. Un dosage radio-enzymatique, approprie pour mesurer les concentrations plasmatiques des derives desamines de la na (3,4-dihydroxyphenyl glycol : dhpg et 3,4-dihydroxymandelique acide : doma) a ete developpe et valide au plan physiologique. Une reduction de l'activite sympathique par la clonidine ou la guanethidine provoque une baisse de la na mais aussi du dhpg ; la reponse du doma est moins claire. Dans une deuxieme etape, nous avons evalue le modele du rat anesthesie, demyele et stimule a 2. 5 hz. Nous avons mesure une baisse du trop-plein synaptique de la na chez le rat demyele, avec retour a la normale quand le rat est stimule. Une correlation a ete calculee entre la concentration plasmatique de la na et celle du dhpg et entre la na et la pression arterielle moyenne suggerant un equilibre synaptique physiologique. Nous avons active la recapture neuronale de la na en perfusant de la na exogene. Le dhpg plasmatique augmente en parallele avec celle de la na ; le doma augmente aussi, mais l'amplitude est moins eleve que celui du dhpg. Quand le metabolisme pre-synaptique est bloque partiellement par la desipramine, le niveau plasmatique du dhpg s'en trouve reduit, mais pas celui du doma. L'inhibition de la monoamine oxydase par la clorgyline (mao-a) ou le deprenyl (mao-b) induit une baisse significative du dhpg (-85%:clorgyline;-74%:deprenyl) et du doma (-30%:clorgyline;-24%:deprenyl). Une inhibition conjointe des mao-a et b conduit a une disparition presque totale du dhpg, mais n'augmente pas la baisse du doma. Globalement, nos resultats demontrent la possibilite d'explorer le metabolisme pre-synaptique de la na chez l'animal entier, le niveau du dhpg pouvant etre un assez bon marqueur de cette voie metabolique.

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10

MAIGNAN, EMMANUELLE. "Systeme sympathique : la cinetique de la noradrenaline chez le rat." Paris 6, 2001. http://www.theses.fr/2001PA066331.

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L'objectif de ce travail a ete d'etudier la physiologie du systeme sympathique chez le rat par la technique de la dilution isotopique (di). Nous avons mesure la cinetique de la noradrenaline (na), definie par son trop plein synaptique (tps) et sa clairance metabolique (cm). Nous montrons que l'anesthesie provoque des alterations majeures et heterogenes de la cinetique de la na. Nous avons d'abord retenu que l'etat experimental qui s'imposait etait le rat conscient, non restreint. Dans ce contexte, son tps est environ 10 fois plus eleve que celui de l'homme, suggerant une activite sympathique beaucoup plus elevee. On peut y associer une sensibilite membranaire presynaptique egalement differente entre ces deux especes. La liberation de la na, mesuree par son tps, peut etre amplifiee par un mecanisme encore mal defini, mais resume par l'expression hypothese adrenaline. Nos resultats montrent bien que l'adrenaline (ad) stimule les recepteurs beta 2-adrenergiques presynaptiques conduisant a une augmentation du tps. Cependant, chez le rat, les niveaux circulants d'ad doivent etre 100 fois superieurs a ceux necessaires chez l'homme pour obtenir le meme effet. Cette liberation peut etre encore plus amplifiee par un niveau d'ad, en lui-meme inefficace, lorsque l'inhibition de la liberation de la na, est partiellement bloquee par la yohimbine. Une stimulation du tps peut etre aussi induite par le formoterol, un beta 2-agoniste de synthese. Notre travail a aussi ete consacre a l'etude de la cm de la na. Nous avons constate qu'une variation experimentale de la na plasmatique ne modifie pas le niveau de la cm de la na tant que l'hemodynamique systemique n'est pas alteree. On peut se demander si les mecanismes, autres que la recapture neuronale, ont vraiment une efficacite dans l'elimination d'un exces de na. Quand la pression arterielle augmente, la cm diminue, demontrant le role predominant de l'hemodynamique dans l'homeostase de la na. Par ailleurs, nous avons etudie la cinetique de la na dans des situations suggerant une hyper- (rats shr) ou une hypoactivite (hypervolemie centrale) sympathique et aussi dans des conditions physiologiques plus particulieres : le rat age ou le rat presentant une surrenalectomie bilaterale. Globalement, nos resultats demontrent l'interet majeur d'explorer l'activite sympathique chez le rat conscient par la technique de di.

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Книги з теми "Noradrenaline"

1

1960-, Fuchs Stefan, and Auer Max 1962-, eds. Biochemistry and histocytochemistry research developments. Hauppauge, N.Y: Nova Science, 2009.

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2

J, Heal David, and Marsden C. A, eds. The Pharmacology of noradrenaline in the central nervous system. Oxford [England]: Oxford University Press, 1990.

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3

Ward, Valerie Lynn. Oxygen-derived free radicals and the pathogenesis of catecholamine cardiomyopathy. [New Haven, Conn: s.n.], 1993.

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4

Singh, Lakhbir. Modulation of a 5-hydroxytryptamine-related behaviour by noradrenaline and gaba. Birmingham: University of Aston. Department of Pharmaceutical Sciences, 1985.

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5

A, Ordway Gregory, Schwartz Michael A, and Frazer Alan, eds. Brain norepinephrine: Neurobiology and therapeutics. Cambridge: Cambridge University Press, 2007.

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6

Pernow, John. Co-release and functional interactions of neuropeptide Y and noradrenaline in peripheral sympathetic vascular control. Oxford: Published for the Scandinavian Physiological Society by Blackwell Scientific Publications, 1988.

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7

Ichishima, Eiji. Unique enzymes of Aspergillus fungi used in Japanese bioindustries. Hauppauge, N.Y: Nova Science Publishers, 2011.

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8

Kirkup, Anthony Joseph. Modulation of membrane currents and mechanical activity by noradrenaline and other agents in vascular smooth muscle. Manchester: University of Manchester, 1995.

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9

Hentschel, Erwin. Occurence and function of biogenic amines (5-hydroxytryptamine, dopamine, noradrenaline, adrenaline and octopamine) in invertebrates: Bibliography = Vorkommen und Funktion biogener Amine (5-hydroxytryptamin, Dopamin, Noradrenalin, Adrenalin und Octopamin) bei wirbellosen Tieren : Bibliographie. Jena: Universitätsbibliothek, 1986.

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10

Hentschel, Erwin. Occurrence and function of biogenic amines (5-hydroxytryptamine, dopamine, noradrenaline, adrenaline and octopamine) in invertebrates: Bibliography = Vorkommen und Funktion biogener Amine (5-hydroxytryptamin, Dopamin, Noradrenalin, Adrenalin und Octopamin) bei wirbellosen Tieren : Bibliographie. Jena: Universitätsbibliothek, 1986.

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Більше джерел

Частини книг з теми "Noradrenaline"

1

Andrews, Anne M., Greg A. Gerhardt, Lynette C. Daws, Mohammed Shoaib, Barbara J. Mason, Charles J. Heyser, Luis De Lecea, et al. "Noradrenaline." In Encyclopedia of Psychopharmacology, 905. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-540-68706-1_715.

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2

Kruk, Zygmunt L., and Christopher J. Pycock. "Noradrenaline." In Neurotransmitters and Drugs, 50–86. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3132-2_3.

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3

Kruk, Zygmunt L., and Christopher J. Pycock. "Noradrenaline." In Neurotransmitters and Drugs, 50–86. Dordrecht: Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3134-6_3.

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4

Pannu, Neesh, Xiaoyan Wen, John A. Kellum, John Fildes, N. Al-Subaie, Mark Hamilton, Susan M. Lareau, et al. "Noradrenaline." In Encyclopedia of Intensive Care Medicine, 1568. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-642-00418-6_1963.

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5

Anagnostou, Evdokia, Deepali Mankad, Joshua Diehl, Catherine Lord, Sarah Butler, Andrea McDuffie, Lisa Shull, et al. "Noradrenaline." In Encyclopedia of Autism Spectrum Disorders, 2053. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1698-3_100948.

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6

Amemiya, Seiichiro. "Noradrenaline." In Encyclopedia of Personality and Individual Differences, 3259–61. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-319-24612-3_785.

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7

Amemiya, Seiichiro. "Noradrenaline." In Encyclopedia of Personality and Individual Differences, 1–3. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-28099-8_785-1.

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8

Segal, Sabrina. "Norepinephrine/Noradrenaline." In Encyclopedia of Behavioral Medicine, 1515. Cham: Springer International Publishing, 2020. http://dx.doi.org/10.1007/978-3-030-39903-0_39.

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9

Tiro, Jasmin, Simon J. Craddock Lee, Steven E. Lipshultz, Tracie L. Miller, James D. Wilkinson, Miriam A. Mestre, Barbara Resnick, et al. "Norepinephrine/Noradrenaline." In Encyclopedia of Behavioral Medicine, 1344–45. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4419-1005-9_39.

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10

Froehlich, Stephan J., Carlo A. Lackerbauer, Guenter Rudolph, Jan Rémi, Soheyl Noachtar, Werner J. Heppt, Annette Cryer, et al. "Noradrenaline Deficiency." In Encyclopedia of Molecular Mechanisms of Disease, 1498. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8067.

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Тези доповідей конференцій з теми "Noradrenaline"

1

Van Diest, M. J., T. J. Verbeuren, and A. G. Herman. "RELAXATIONS INDUCED BY LIPOXYGENASE METABOLITES OF ARACHI-DONIC ACID IN SPLENIC ARTERIES OF THE DOG." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643796.

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The lipoxygenase metabolites of arachidonic acid, 15 hydroperoxyeicosatetraenoic acid (15HPETE) and its hydroxy derivative (15HETE) evoke contractions in a variety of isolated blood vessels. We recently were able to show that thromboxane A2 (TXA2)-receptor antagonists BM13177 and BM13505 suppress the contractions induced by lipoxygenase metabolites in canine splenic arteries, and that these compounds also inhibit the contractile effects of PGF2α and of the TXA2-mimetic U46619. We also reported that 15HETE and 15HPETE cause relaxations of isolated dog arteries when the tissues are contracted with prostaglandin F2α (PGF2α) or with U46619 and suggested that lipoxygenase metabolites may act as endogenous antagonists towards prostaglandin receptors. The present study was designed to investigate the effects of lipoxygenase metabolites of arachidonic acid in isolated splenic arteries in which the tone is raised by various agonists.Segments of canine splenic arteries with or without endothelium were placed in organ chambers filled with Krebs-Ringer solution at 37°C for isometric tension recording. Responses to 15HPETE were obtained in segments which were contracted with serotonin, K+, PGF2α or noradrenaline (the latter with or without BM13505); concentrations causing comparable levels of contraction were selected. HPETE evoked relaxations in segments with and without endothelium, during the contractions evoked by K+, PGF2α and noradrenaline (with or without BM13505). At higher concentrations, 15HPETE caused relaxations only during contractions induced by PGF2α and noradrenaline with BM13505. Our results suggest that 15HPETE can cause relaxations by two different mechanisms :(1) 15HPETE may act as an antagonist to PGF2α, which causes its contraction via the TXA2-receptor and,(2) in presence of BM13505, it suppresses the contractions to noradrenaline via an endothelium independent mechanism.

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2

Carrere, Maxime, and Frederic Alexandre. "Modeling the sensory roles of noradrenaline in action selection." In 2016 Joint IEEE International Conference on Development and Learning and Epigenetic Robotics (ICDL-EpiRob). IEEE, 2016. http://dx.doi.org/10.1109/devlrn.2016.7846814.

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3

Ishikawa, G., X. Peng, J. Mcgovern, A. Ghincea, T. Saber, H. Sun, M. Sauler, C. Ryu, and E. Herzog. "Role of Noradrenaline and Macrophage Dynamics in Pulmonary Fibrosis." In American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a5206.

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4

Hesse, S., C. Ulke, M. Rullmann, J. Luthardt, J. Huang, GA Becker, M. Patt, et al. "Prefrontal-thalamic noradrenaline transporter availability is reduced in adults with ADHD." In NuklearMedizin 2019. Georg Thieme Verlag KG, 2019. http://dx.doi.org/10.1055/s-0039-1683515.

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5

Chung, Hui-Kuan, and Philippe Tobler. "Boosting noradrenaline improves economic rationality by enhancing attention in healthy humans." In 2023 Conference on Cognitive Computational Neuroscience. Oxford, United Kingdom: Cognitive Computational Neuroscience, 2023. http://dx.doi.org/10.32470/ccn.2023.1463-0.

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6

Sun, H., C. Perry, A. Ghincea, T. Baernthaler, and E. Herzog. "Reduction in Systemic Noradrenaline Does Not Suppress Bleomycin Induced Lung Fibrosis." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1943.

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7

BRINK, K., F. DERKX, E. BROMMER, J. STIBBE, H. KOLSTEE, and M. SCHALEKAMP. "THE FIBRINOLYTIC, FACTOR VIII:C, VON WILLEBRAND FACTOR AND HEMODYNAMIC RESPONSES TO DDAVP IN PATIENTS WITH HEREDITARY NEPHROGENIC DIABETES INSIPIDUS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644709.

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The pressor response of vasopressin (AVP) is mediated by a calcium-dependent mechanism (VI-receptor), whereas its antidiuretic effect depends on c-ANP (V2-receptor). DDAVP (1-desamino-8-D-arginine vasopressin) is a synthetic V2 analog of AVP. AVP and DDAVP also increase FVIII:C vWF:Ag and tissue-type plasminogen activator (t-PA) in plasma. The mechanism by which AVP and DDAVP elevate these factors is unclear. Patients with X-linked nephrogenic diabetes insipidus (NDI) are resistant to the V2-mediated antidiuretic action of AVP and DDAVP. We therefore have studied the effect of DDAVP (0.4 ug/kg iv infusion in 10 min) in 2 brothers with NDI, their mother and an unrelated patient.In control subjects (n=12) FVIII:C rose 122 (6) % ,mean (SEM), vWF:Ag 104 (4) % and t-PA 115 (7) % over basal levels. This rise was associated with a fall in diascolic blood pressure -11 (3) mmHg and an increase in heart rate from 62 (4) to 91 (5) bpm. Plasma noradrenaline rose from 262 (34) to 590 (84) pg/ml and renin from 16 (3) to 42 (6) uU/ml. Ten out of 12 controls showed facial flusning. The patients with NDI had normal basal FVIII:C, vWF:Ag and t-PA levels. Plasma noradrenaline and renin were within the nor mam range. Tne patients with NDI were also resistant to the stimulatory effect of DDAVP on the release of FVIII:C, vWF:Ag and t-PA. They also showed no change in blood pressure, nearc rate, plasma noradrenaline and renin and had no facial flushing. The carrier had normal responses to DDAVP.Tne increase in FVII:C, vWF:Ag and t-PA and the hemodynamic responses after DDAVP infusion probably appear to depend on extrarenal V2-receptor activation. DDAVP cannot be used in identifying carriers in families at risk.

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8

Schmidt, E., C. Schinke, M. Rullmann, J. Luthardt, GA Becker, S. Haars, M. Stoppe, et al. "Changes of central noradrenaline transporter availability in immunotherapy-naïve multiple sclerosis patients." In NuklearMedizin 2020. © Georg Thieme Verlag KG, 2020. http://dx.doi.org/10.1055/s-0040-1708189.

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9

Morais, Camila, Dora Kassisse, Filipy Borghi, Carolina da Silva, and Priscila da Silva. "Signaling downstream cascade crosstalk induced by noradrenaline on angiotensin II metabolic activity in adipocytes." In Congresso de Iniciação Científica UNICAMP. Universidade Estadual de Campinas, 2019. http://dx.doi.org/10.20396/revpibic2720191878.

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10

Lanza, M., A. Beretz, A. Stierlé, D. Hanau, M. Kubina, and J. P. Cazenave. "ADRENALINE ACTIVATES HUMAN PLATELETS BUT IS NOT PER SE AN AGGREGATING AGENT. EFFECTS ON PLATELET MORPHOLOGY, MEMBRANEFLUIDITY, FIBRINOGEN BINDING, CYTOPLASMIC FREE CALCIUM AND PROTEIN PHOSPHORYLATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643762.

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Adrenaline (Adr) is generally considered as a full agonist able to induce in vitro the aggregation of human platelets and could play an important role in vivo in the appearance of thrombotic disorders when catecholamine levels are increased. Adr 2.5 M) induces the aggregation and secretion of 41 % of preloaded 3H-serotonin in human platelets in citrated plasma. This effect is not seen in plasma collected on 50 ATU/ml hirudin, and is due to the generation of traces of thrombin during blood collection and not to a direct effect of citrate itself, such asthe lowering of plasma free calcium. With washed human platelets suspended in Tyrode's buffer containing 2 mM Ca2+, 0.35 %albumin and apyrase, Adr (0.1 -100 M) doesnot cause shape change, aggregation or secretion of serotonin and does not modify platelet ultrastructure as judged by electron microscopy. Adr (1-100 M) does not change platelet membrane fluidity, as studied with the lipophilic fluorescent probe TMA-DPH. Adr has no direct effect on fibrinogen binding to intact platelets, intracellular Ca2+levels measured with quin2, or phosphorylation of 20 KDa or 47 KDapolypeptides, whereas all these parameters are modified after stimulation with ADP orthrombin. Adr potentiates the action of all types of aggregating agents on aggregation, secretion, intracellular Ca2+ levels,membrane fluidity, fibrinogen binding or protein phosphorylation. This effect is also seen with alpha2-adrenergic agonists (noradrenaline, alpha-methyl noradrenaline, clonidine) and is inhibited by alpha2-adrenergicantagonists such as yohimbine. The potentiation of platelet aggregation by Adr is not modified by prior incubation of the platelets with1mM aspirin for 15 min. This study shows that Adr alone does not induce modifications ofmorphology, metabolism or function of intactand functional washed human plateletsand that Adr cannot be considered per se as an aggregating agent. However, Adr interactswith alpha2-adrenergic receptors on human plateletsand potentiates biochemical and aggregatory responses induced by other platelet agonists.

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Звіти організацій з теми "Noradrenaline"

1

Noradrenaline confirmed as first-choice vasopressor for septic shock. National Institute for Health Research, December 2015. http://dx.doi.org/10.3310/signal-000165.

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