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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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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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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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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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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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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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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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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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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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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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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 (June 1, 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 experiments in vitro averaged 16% at room temperature. 4. With tyramine added to the perfusates, noradrenaline levels increased 10-fold. Arterial noradrenaline concentrations did not change, indicating that noradrenaline was released only locally in the tissue. 5. Our results indicate that the microdialysis technique combined with a sensitive assay for measuring noradrenaline may be applicable to the assessment of local noradrenaline release in adipose tissue and in skeletal muscle. This may be of interest, especially in adipose tissue during physiological stimulation in which sympathetic activity is difficult to evaluate by other techniques.
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Nutt, David. "Noradrenaline revisited." Journal of Psychopharmacology 5, no. 4 (July 1991): 442–44. http://dx.doi.org/10.1177/026988119100500444.
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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 (November 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 the species in the intralobular distribution of noradrenaline-immunoreactive fibres. Normal guinea-pig and human liver showed intralobular noradrenaline-immunoreactive fibres while rat liver did not. Noradrenaline-immunoreactive fibres were absent from regenerating nodules in a human cirrhotic liver. This method of demonstrating noradrenaline directly using perfusion- or immersion-fixation is appropriate for studying innervation in normal and damaged livers of various species including humans.
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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 (August 1985): 105–9. http://dx.doi.org/10.1016/0304-3940(85)90222-8.
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Inokuchi, Hiroe, Megumu Yoshimura, Canio Polosa, and Syogoro Nishi. "Adrenergic receptors (α1 and α2) modulate different potassium conductances in sympathetic preganglionic neurons." Canadian Journal of Physiology and Pharmacology 70, S1 (May 15, 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 depolarization was associated with an increase in neuron input resistance, while the noradrenaline-induced hyperpolarization was associated with a decrease in neuron input resistance. Both responses decreased in amplitude with membrane hyperpolarization and were nullified at around the potassium equilibrium potential EK. The null potential of both responses became more and less negative with a decrease and an increase, respectively, in the extracellular potassium concentration. When the membrane potential was made more negative than EK, the noradrenaline-induced hyperpolarization reversed to depolarization in all cases, whereas in only 4 of 12 cases did the noradrenaline-induced depolarization reverse to hyperpolarization. These data suggest that the noradrenaline-induced depolarization is a result of a decrease, while the noradrenaline-induced hyperpolarization is a result of an increase in K+ conductance. Cobalt (2 mM), low calcium – high magnesium, and intracellular EGTA markedly reduced or abolished the noradrenaline-induced depolarization but had no significant effect on the noradrenaline-induced hyperpolarization. Barium (2 mM) depressed both responses. Tetraethylammonium (10–30 mM), 4-aminopyridine (3 mM), and cesium (2 mM) had no effect on either response. These data suggest that the noradrenaline-induced depolarization is a result of an inactivation of a background calcium-sensitive K+ conductance, while the noradrenaline-induced hyperpolarization is due to activation of a calcium-insensitive potassium conductance.Key words: K+ conductances, catecholamines, Ca2+ dependent, K+ current, spinal cord.
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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 (March 1, 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 uptake, even in the absence of insulin. The effects of noradrenaline and insulin on dGlc uptake were additive. The stimulatory effect of noradrenaline was mimicked by the β3-adrenergic agonist, BRL37344, at concentrations two orders lower than noradrenaline. Dibutyryl cyclic AMP also mimicked the stimulatory effect of noradrenaline, and the antagonist of cyclic AMP, cyclic AMP-S Rp-isomer, blocked the enhancement of glucose uptake due to noradrenaline. Furthermore Western blot analysis with an anti-phosphotyrosine antibody revealed that, in contrast with insulin, noradrenaline apparently does not stimulate intracellular phosphorylation of tyrosine, suggesting that the noradrenaline-induced increase in dGlc uptake depends on elevation of the intracellular cyclic AMP level and not on the signal chain common to insulin. When cells were incubated with insulin, the content of the muscle/adipocyte type of glucose transporter (GLUT4) in the plasma membrane increased, with a corresponding decrease in the amount in the microsomal membrane. In contrast, noradrenaline did not affect the subcellular distribution of GLUT4 or that of the HepG2/erythrocyte type of glucose transporter. Although insulin increased Vmax. and decreased the Km value for glucose uptake, the effect of noradrenaline was restricted to a pronounced decrease in Km. These results suggest that the mechanism by which noradrenaline stimulates glucose transport into brown adipocytes is not due to translocation of GLUT but is probably due to an increase in the intrinsic activity of GLUT, which is mediated by a cyclic AMP-dependent pathway.
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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 (December 22, 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 contractions without any effect on the local concentration of noradrenaline, as measured by microdialysis, and noradrenaline spillover. Fractional extraction of both noradrenaline and adrenaline was unaffected by increasing blood flow three and four times its resting value. In addition, noradrenaline spillover was increased by the higher blood flow, from 188 to 452 pg·min-1 at rest and from 246 to 880 pg·min-1 during stimulation. Stimulation of muscle contraction caused a significant increase in fractional extraction of noradrenaline and a nonsignificant increase in adrenaline extraction. In addition, an adrenaline spillover was observed in certain conditions. In light of our results, it seems that blood flow may not be the main factor decreasing fractional extraction of noradrenaline during exercise. However, blood flow could contribute to the increase in noradrenaline spillover observed in the active muscles during exercise.Key words: skeletal muscle, spillover, fractional extraction, stimulation, adrenaline.
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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 (November 1, 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 pressure were found at arterial and venous plasma noradrenaline concentrations (means ±sem) of 3.00 ± 0.23 and 1.35 ±0.12 nmol/l, respectively. A significant decrease in heart rate was found at arterial and venous plasma noradrenaline concentrations of 8.99 ± 0.69 and 3.09 ± 0.60 nmol/l, respectively. The lower doses of noradrenaline tended to increase forearm blood flow and to decrease forearm vascular resistance, whereas the higher doses had no consistent effect on forearm haemodynamics. 4. During the noradrenaline infusions 73 ± 5% of the increase in arterial plasma noradrenaline concentration was extracted in the forearm. 5. The venous plasma noradrenaline threshold concentration was found to be much lower than previously reported. It is concluded that arterial and venous plasma noradrenaline concentrations which are readily encountered in physiological circumstances elicit haemodynamic effects.
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McCance, Alastair J., and J. Colin Forfar. "Cardiac and Whole-Body [3H]Noradrenaline Kinetics during Adrenaline Infusion in Man." Clinical Science 80, no. 3 (March 1, 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 pg/ml to 245 ± 29 pg/ml (P < 0.05). Increases in whole-body noradrenaline spillover to arterial plasma were larger (from 282 ± 40 ng min−1 m−2 to 358 ± 41 ng min−1 m−2, P < 0.01) and there was a trend towards an increase in whole-body noradrenaline clearance. Cardiac noradrenaline clearance was modestly increased during adrenaline infusion, but cardiac noradrenaline spillover was not altered despite increases in heart rate and coronary sinus plasma flow. Adrenaline infusion was associated with symptomatic myocardial ischaemia in four of 14 patients with coronary heart disease. 3. Supine bicycle exercise was associated with significant increases in peripheral noradrenaline concentrations and in cardiac and whole-body noradrenaline spillover. The increases on exercise were not significantly different for these variables during saline and adrenaline infusions. 4. Infusion of adrenaline to produce ‘physiological’ increases in plasma adrenaline concentration was associated with an increase in total noradrenaline release, as assessed by whole-body noradrenaline spillover to plasma. This is consistent with the hypothesis that adrenaline may modulate noradrenaline release by acting upon pre-junctional β-adrenoceptors, but could also be explained by reflexogenic responses to the haemodynamic effects of adrenaline.
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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 (November 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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Bacon, Travis J., Anthony E. Pickering, and 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, no. 12 (July 1, 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 mouse hippocampal CA1 pyramidal neurons. We show that endogenous noradrenaline release enhances the probability of CA1 pyramidal neuron spiking without altering feedforward excitatory or inhibitory synaptic inputs in the Schaffer collateral pathway. β-adrenoceptors mediate this enhancement of excitation-spike coupling by reducing the charge required to initiate action potentials, consistent with noradrenergic modulation of voltage-gated potassium channels. Furthermore, we find the likely effective concentration of endogenously released noradrenaline is sub-micromolar. Surprisingly, although comparable concentrations of exogenous noradrenaline cause robust depression of slow afterhyperpolarization currents, endogenous release of noradrenaline does not, indicating that endogenous noradrenaline release is targeted to specific cellular locations. These findings provide a mechanism by which targeted endogenous release of noradrenaline can enhance information transfer in the hippocampus in response to salient events.
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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 (March 20, 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 group) was injected into the uterine horns. Eight days later, severe acute endometritis developed in the E. coli group. Endometrial explants were incubated with noradrenaline and/or α1-, α2- and β-AR antagonists. In the CON group, noradrenaline did not significantly change PTGS-2 and mPTGES-1 protein expression and increased PGE2 secretion compared to the control values (untreated tissue). In the E. coli group, both enzyme expression and PGE2 release were stimulated by noradrenaline, and these values were higher versus the CON group. The antagonists of α1- and α2-AR isoforms and β-AR subtypes do not significantly alter the noradrenaline effect on PTGS-2 and mPTGES-1 protein levels in the CON group, compared to noradrenaline action alone. In this group, α1A-, α2B- and β2-AR antagonists partly eliminated noradrenaline-stimulated PGE2 release. Compared to the noradrenaline effect alone, α1A-, α1B-, α2A-, α2B-, β1-, β2- and β3-AR antagonists together with noradrenaline reduced PTGS-2 protein expression in the E. coli group. Such effects were also exerted in this group by α1A-, α1D-, α2A-, β2- and β3-AR antagonists with noradrenaline on mPTGES-1 protein levels. In the E. coli group, the antagonists of all isoforms of α1-ARs and subtypes of β-ARs as well as α2A-ARs together with noradrenaline decreased PGE2 secretion versus noradrenaline action alone. Summarizing, in the inflamed pig endometrium, α1(A, B)-, α2(A, B)- and β(1, 2, 3)-ARs mediate the noradrenaline stimulatory effect on PTGE-2 protein expression, while noradrenaline via α1(A, D)-, α2A- and β(2, 3)-ARs increases mPTGES-1 protein expression and α1(A, B, D)-, α2A- and β(1, 2, 3)-ARs are involved in PGE2 release. Data suggest that noradrenaline may indirectly affect the processes regulated by PGE2 by influencing its production. Pharmacological modulation of particular AR isoforms/subtypes can be used to change PGE2 synthesis/secretion to alleviate inflammation and improve uterine function.
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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 (November 1, 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 otherwise healthy patients with moderate degrees of low-output cardiac failure and in six normal control subjects. 4. The venous plasma noradrenaline level was elevated in the patients with congestive heart failure as compared with the control subjects (4.18±1.34 versus 1.54 ± 0.16 nmol/l, P < 0.05). There was no stimulation of the adrenal medulla as evident by normal plasma adrenaline levels in both groups (0.19 ±0.04 versus 0.1810.02 nmol/l, not significant). The apparent secretion rate of noradrenaline was elevated in the patients with congestive heart failure (4.75 ±1.95 versus 1.78±0.18 nmol min−1 m−2, P < 0.05), whereas the clearance rate of noradrenaline was similar in the two groups (1.26±0.27 versus 1.16±0.02 1 min−1 m−2, not significant). 5. We conclude that the high peripheral venous plasma noradrenaline concentrations in patients with mildly decompensated low-output cardiac failure are initially due to increased secretion, rather than to decreased metabolic clearance, perhaps in response to diminished effective arterial blood volume.
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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 (January 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 concentration were observed in both normal subjects and hypercholesterolaemic patients. 5. Combining the data for normal subjects and hypercholesterolaemic patients revealed that the plasma noradrenaline concentration correlated positively with the plasma cholesterol concentration. The platelet noradrenaline concentration was also found to correlate with the plasma cholesterol concentration. 6. Our results suggest that an increased plasma cholesterol concentration may be associated with increased sympathetic nervous system activity as indicated by elevated plasma and platelet noradrenaline levels. Increases in circulating catecholamines may contribute to the platelet hyperaggregability seen in familial hypercholesterolaemia.
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Cañas, N., D. Sanchis, G. Gómez, J. M. Casanovas, F. Artigas, J. A. Fernández-López, X. Remesar, and X. Alemany. "3-Hydroxybutyrate co-infused with noradrenaline decreases resulting plasma levels of noradrenaline in Wistar rats." Journal of Experimental Biology 200, no. 20 (October 1, 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 brown adipose tissue temperatures increased with noradrenaline infusion, but the rise was arrested by 3-OHB; replacing 3-OHB with glucose had no effect. Infusion of saline, glucose or 3-OHB in the absence of noradrenaline did not induce a rise in temperature in either tissue. Blood 3-OHB concentration increased to 1.2 mmoll-1 during 3-OHB infusion, decreasing rapidly at the end of infusion. Blood glucose levels increased with noradrenaline infusion; the presence of high 3-OHB levels decreased glucose concentration. The effects observed were transient and dependent on 3-OHB concentration; these effects may help explain most of the other effects of noradrenaline described here. The role of 3-OHB as a regulator of adrenergic responses seems to be part of a complex fail-safe mechanism which prevents wasting.
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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 (February 1, 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 µmol 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 µmol l-1) before, simultaneously with or after reduction of osmolality (255 mosmol kg-1), the volume regulatory efflux of taurine mediated by the taurine channel was transiently accelerated. The rate coefficient for taurine efflux was more than four times higher than in osmolality-stimulated cells not exposed to noradrenaline. The present paper deals with the accelerating effect of noradrenaline on the taurine channel under hypo-osmotic conditions and the lack of effect of noradrenaline-induced cell swelling on the channel under iso-osmotic conditions. Noradrenaline initiated the cell swelling by interacting with ß-receptors which appeared to be more related to the mammalian ß1-receptors than to the ß2-receptors. The receptor interaction activated the adenylate cyclase system and, in the presence of 1.0 µmol l-1 noradrenaline, the cellular cyclic AMP concentration increased about 23 times. Noradrenaline also stimulated the Na+/H+ and Cl-/HCO3- antiporters and this affected the extracellular pH as well as the cell volume. Depending on the extracellular Na+ concentration, the incubation medium was acidified (113 mmol l-1 Na+) or alkalized (2.7 mmol l-1 Na+). Under these two conditions, the accelerating effects of noradrenaline on the taurine efflux were of similar magnitude. Similar effects on the cell volume, the extracellular pH and the volume regulatory taurine efflux were obtained in the presence of the cyclic AMP analogue 8-bromo-cyclic AMP. Under hypo-osmotic conditions in the absence of noradrenaline, the cellular level of cyclic AMP was not elevated. There was no significant positive correlation between the water content of the cells (cell volume) under different conditions in the presence or absence of noradrenaline and the state of activation of the osmolality-sensitive taurine channel. We conclude that the mechanism(s) which activate(s) the osmolality-sensitive taurine channel in flounder erythrocytes is transiently and strongly accelerated by noradrenaline, but not triggered by the noradrenaline-induced events. The acceleration does not appear to be due to increased activity of the antiporters, but to increased cellular levels of cyclic AMP.
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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 (March 1989): 191–92. http://dx.doi.org/10.1177/000456328902600219.
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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 (December 1, 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 magnitude of the noradrenaline response in arteries from both control and diabetic rats. These data confirm the selective nature of the enhancement of contractile responses of arteries from diabetic rats to noradrenaline and suggest that this may be mediated in part through enhanced noradrenaline-induced influx of extracellular Ca2+ through channels sensitive to the Ca2+ channel ligands. However, this does not appear to be the only explanation for the enhanced contractile responses of diabetic arteries to noradrenaline, since in the presence of maximum concentrations of nifedipine (3 μM) and verapamil (10μM), responses of diabetic arteries to noradrenaline were still greater than those of control arteries.Key words: diabetes, arteries, contractility, noradrenaline, extracellular Ca2+.
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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 (March 1, 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 that the response was mediated by alpha 2-adrenergic receptors. Noradrenaline significantly reduced the extent of 45Ca2+ accumulation in glucose-stimulated islets, although as much as 5 microM-noradrenaline was required for 50% inhibition of this response. The ability of noradrenaline to inhibit islet-cell 45Ca2+ uptake was totally abolished in media containing 1 mM-dibutyryl cyclic AMP, suggesting that the response may have been secondary to lowering of islet cyclic AMP. Under these conditions, however, noradrenaline was still able to inhibit insulin secretion maximally. The data suggest that the site(s) at which noradrenaline acts to mediate inhibition of insulin secretion in rat islets lies distal to both islet-cell cyclic AMP accumulation and Ca2+ uptake.
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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 (October 1, 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 effect of increasing noradrenaline release and decreasing noradrenaline clearance. 3. Alcohol caused a transient rise in erect and supine blood pressures that preceded the rise in plasma noradrenaline. Thereafter erect blood pressures fell compared with control. This fall was associated with a progressive rise in both supine and erect rates, and reached a maximum several hours after the maximum levels of blood alcohol. 4. The major effect of acute alcohol administration is to lower blood pressure and induce a reflex tachycardia. Changes in noradrenaline and 3,4-dihydroxyphenylethylene glycol levels did not readily explain changes in blood pressure or heart rate, suggesting that alcohol induced changes in noradrenaline metabolism occur largely independent of changes in blood pressure and heart rate.
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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 (June 1, 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 incubation medium in both normal and diabetic subjects. Supernatant noradrenaline concentrations obtained under thrombin-stimulated conditions did not significantly differ between normal and diabetic subjects. However, under resting conditions noradrenaline levels were significantly greater (+ 93%, P < 0.02) for diabetic than normal subjects. 4. Measurement of platelet noradrenaline contents after thrombin stimulation revealed no difference between normal and diabetic subjects. Under resting conditions, however, platelet noradrenaline levels were significantly lower (−46%, P < 0.02) for diabetic than normal subjects. Thus, in the diabetic subjects increased resting platelet efflux of noradrenaline is mirrored by a decreased platelet noradrenaline content. 5. A consequence of increases in resting catecholamine efflux may be enhanced platelet activity resulting in increased platelet aggregation.
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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 (June 22, 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 characterize the purinergic modulation of noradrenaline release evoked by NMDARs. Stimulation of rat cortical slices with 30 µM NMDA increased noradrenaline release, which was inhibited by ATP upon metabolization into ADP and adenosine and by the selective agonists of A1 and A2A receptors, CPA and CGS2680, respectively. It was also inhibited by UTP and UDP, which are mainly released under pathophysiological situations. Characterization of the effects mediated by these compounds indicated the involvement of P2Y1, P2Y6, A1 and A2A receptors. It is concluded that, in the rat brain cortex, NMDA-evoked noradrenaline release is modulated by several purinergic receptors that may represent a relevant mechanism to regulate the permissive effect of noradrenaline on NMDA-induced neuroplasticity.
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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 (October 1, 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 gracilis muscle, using the specific B2 antagonist HOE 140. The drug did not modify noradrenaline spillover at rest, but did cause a significant decrease during muscle contraction, from 558 to 181 pg·min1. As reported previously in the literature, fractional extraction of noradrenaline decreased during muscle contraction. This effect was independent of HOE 140 treatment. In light of our results, it seems that bradykinin formation during muscle contraction may play an important part in the observed increase in noradrenaline spillover but does not affect fractional extraction.Key words: skeletal muscle, fractional extraction, stimulation, HOE 140, B2 receptors.
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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 (September 1, 1986): 395–403. http://dx.doi.org/10.1042/bj2380395.
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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-stimulated respiration in rat brown adipocytes. Hypothyroidism diminished the maximum response of respiration and lipolysis to noradrenaline in rat cells and increased the EC50 for noradrenaline. Responsiveness of lipolysis to noradrenaline was particularly decreased in hypothyroidism and was partially restored by addition of adenosine deaminase. Lipolysis in cells from hypothyroid rats was more sensitive to the anti-lipolytic action of PIA. Bordetella pertussis toxin increased lipolysis in the presence of PIA, suggesting an involvement of the Ni guanine-nucleotide-binding protein in the control of brown-adipocyte metabolism.
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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 (April 1, 1998): 383–93. http://dx.doi.org/10.1042/cs0940383.
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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 systolic blood pressure and heart rate increased significantly and diastolic blood pressure decreased. Total noradrenaline spillover, and arterial and coronary sinus plasma noradrenaline concentrations, increased significantly. Muscle sympathetic nerve traffic increased both during and after the end of the infusion. 3. Thirty minutes after the end of the adrenaline infusion there was adrenaline release from the heart (1.5 ± 0.4 ng/min, mean ± S.E.M.) indicating that significant adrenaline loading of cardiac sympathetic nerves had occurred. At this time muscle sympathetic nerve traffic and total body and cardiac noradrenaline spillovers were similar (P > 0.05) to pre-adrenaline infusion values (nerve traffic 24 ± 4 versus 21 ± 3 bursts/min; total noradrenaline spillover 698 ± 98 versus 618 ± 119 ng/min; cardiac noradrenaline spillover 16.2 ± 2.8 versus 13.9 ± 3.9 ng/min). 4. Isometric handgrip contraction evoked similar responses pre- and post-adrenaline infusion in total and cardiac noradrenaline spillovers and in muscle sympathetic activity. 5. The results do not support the theory that adrenaline is a co-transmitter facilitating noradrenaline release from human sympathetic nerves.
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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 (November 1, 1996): 621–26. http://dx.doi.org/10.1042/cs0910621.
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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, whereas plasma noradrenaline increased slightly but significantly with age. Physical training did not influence either plasma noradrenaline or adrenaline at rest or cAMP in lymphocytes. 4. In seven elderly long-term smokers cAMP production and the viability of lymphocytes were reduced. Plasma noradrenaline attained its highest values in long-term smokers. 5. It is concluded that cAMP production and plasma noradrenaline are related to lymphocyte subset composition. The greater the proportion of natural killer cells and related subsets, the higher is cAMP production and the lower is plasma noradrenaline. Thus, the inverse correlation between lymphocyte cAMP and plasma noradrenaline is indirect and most likely mediated by variability in lymphocyte subset composition. In elderly subjects, reduced cAMP production was observed in long-term smokers, and this abnormality was probably due to a reduced viability of lymphocytes and especially of natural killer cells. The negative correlation between the proportion of natural killer cells and plasma noradrenaline at rest contrasts with a well-known mobilizing effect of adrenaline on natural killer cells.
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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 (September 1, 1998): 377–83. http://dx.doi.org/10.1042/cs0950377.
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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 noradrenaline concentration in LP which could be ascribed to residual thrombocytes, calculated from the average noradrenaline concentration in thrombocytes and the number of thrombocytes in LP, correlated closely to noradrenaline in LP (P< 0.007). 3.To test the hypothesis that noradrenaline in LP was primarily derived from plasma, we studied three patients with phaeochromocytoma, who had high levels of noradrenaline and adrenaline both in plasma and in LP. 4.Further studies showed that the addition of thrombocytes to LP increased cAMP. The response was inhibited by indomethacin, whereas the addition of cimetidine and propranolol had no effect on basal or thrombocyte-stimulated cAMP. 5.We conclude that noradrenaline in LP is a marker of the number of residual thrombocytes. The addition of thrombocytes to LP increased cAMP in lymphocytes. This response was not mediated by catecholamines but possibly by prostaglandins.
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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 (August 1990): 493–99. http://dx.doi.org/10.1017/s0033291700017001.
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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 compared to cortisol suppressors. We determined significantly positive correlations between the postdexamethasone cortisol values and the excretion rates of noradrenaline and VMA. These indices of noradrenaline activity correlated neither with the baseline cortisol and ACTH nor with the postdexamethasone ACTH values.
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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 (July 1, 1985): 1–6. http://dx.doi.org/10.1042/cs0690001.
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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 positively correlated with age. 6. Determination of platelet factors released to the plasma showed increases of β-thromboglobulin and platelet factor 4 with exercise, whereas thromboxane B2 remained unchanged. No change in platelet catecholamine levels occurred with exercise and no correlations were observed between platelet catecholamines and released platelet factors. 7. These data suggest that plasma catecholamine levels influence platelet content and that noradrenaline and adrenaline are concentrated in platelets.
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Kelly, C. B., and S. J. Cooper. "Plasma noradrenaline response to electroconvulsive therapy in depressive illness." British Journal of Psychiatry 171, no. 2 (August 1997): 182–86. http://dx.doi.org/10.1192/bjp.171.2.182.
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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 plasma noradrenaline and Cortisol. Clinical ratings were carried out weekly during the course of ECT.ResultsPlasma noradrenaline fell significantly in those patients with melancholic/psychotic depressions but increased in those with non-melancholic depressive illness. There was a strong trend indicating that a fall in plasma noradrenaline was associated with improvement in depression ratings in the melancholic/psychotic patients only.ConclusionsElectroconvlusive therapy decreases plasma noradrenaline in melancholic/psychotic depressive illness and this shows a trend associated with clinical improvement.
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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 (June 23, 2004): 89–95. http://dx.doi.org/10.1042/cs20030355.
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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 adrenaline (epinephrine), noradrenaline (norepinephrine) and cortisol were dichotomized to perform multivariate analyses of (co)variance. Haemostatic parameters were measured by ELISA. Fibrinogen was higher in men with high adrenaline (F7,631=5.68, P=0.018; where the subscripted value represents the degrees of freedom) and high noradrenaline (F7,631=4.19, P=0.041) compared with men with low excretion of the respective hormones. PAI-1 was higher in men with high cortisol than in men with low cortisol (F7,631=4.77, P=0.029). Interaction revealed that subjects with high cortisol/low noradrenaline had higher PAI-1 than subjects with low cortisol/high noradrenaline (P=0.038). Subjects with high adrenaline/high noradrenaline had higher D-dimer than subjects with high adrenaline/low noradrenaline (P=0.029), low adrenaline/high noradrenaline (P=0.022) and low adrenaline/low noradrenaline (not significant). When covariance for several confounders of haemostatic function was determined, the main effect of adrenaline on fibrinogen and the interaction between adrenaline and noradrenaline for D-dimer maintained significance. Although overnight SNS hyperactivity was associated independently with morning hypercoagulability, the relationship between the activity of HPAA and haemostasis was mediated by traditional cardiovascular risk factors.
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Lee, DongJin R., Natalie J. Galant, Donghoon M. Lee, Sean S. H. Dawson, Vanna Z. Y. Ding, David H. Setiadi, Bela Viskolcz, and Imre G. Csizmadia. "Theoretical investigation of the conformational intricacies and thermodynamic functions of noradrenaline." Canadian Journal of Chemistry 89, no. 8 (August 2011): 1010–20. http://dx.doi.org/10.1139/v11-076.
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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 specific role that the catechol ring hydroxyl groups might play in stabilizing noradrenaline, the quantum chemical computations of geometry optimization and thermodynamic functions of N-protonated noradrenaline conformers were performed at both the B3LYP/6–31G(d,p) and G3MP2B3 levels of theory, using the Gaussian 03 program. The results were compared with those of N-protonated β-hydroxy-β-phenylethylamine, which is identical to noradrenaline except it lacks two catechol ring hydroxyl groups. For the first time, post-Hartree–Fock computations were used to obtain thermodynamic functions to establish relative stabilities of all possible conformers of N-protonated noradrenaline. In this study, 18 distinct structures of N-protonated noradrenaline were revealed, and the catechol ring hydroxyl groups were found to affect noradrenaline stability positively or negatively depending on the conformational orientations. On the basis of available experimental results, the issue that the least stable conformation of two catechol ring hydroxyl groups may be involved in the docking process has been raised. These findings may be useful in synthesis of derivatives of noradrenaline in drug design.
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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 (January 1, 1988): 267–80. http://dx.doi.org/10.1242/jeb.134.1.267.
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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 noradrenaline and adrenaline, respectively. Winter fish showed a red cell adrenergic response identical to that of summer-acclimated fish. It is concluded that most red cell beta-adrenergic responses in vivo are exclusively elicited by noradrenaline.
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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 (June 7, 2024): 6313. http://dx.doi.org/10.3390/ijms25126313.
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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 (CON group) was injected into the uterine horns. In both groups, noradrenaline increased endometrial PGIS abundance and PGI2 release versus the control values, and it was higher in the E. coli group than in the CON group. In the CON group, a noradrenaline stimulating effect on both parameters takes place through α1D-, α2C- and β2-ARs. In the E. coli group, noradrenaline increased PGIS abundance and PGI2 release via α1A-, α2(B,C)- and β(1,2)-ARs, and PGI2 release also by α2A-ARs. Experiment 2. LPS and noradrenaline augmented the examined parameters in endometrial epithelial cells versus the control value. In LPS-treated cells, β(1,2)-ARs mediate in noradrenaline excitatory action on PGIS protein abundance and PGI2 release. β3-ARs also contribute to PGI2 release. Under inflammatory conditions, noradrenaline via ARs increases PGI2 synthesis and release from the porcine endometrium, including epithelial cells. Our findings suggest that noradrenaline may indirectly affect processes regulated by PGI2 in the inflamed uterus.
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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 (May 1, 1996): 337–43. http://dx.doi.org/10.1042/cs0900337.
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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 negative pressure at −15 mmHg, heart rate and pulse pressure did not change, but forearm vascular resistance increased by 25–50%. Forearm noradrenaline spillover increased by about 50%, from 0.63 ± 0.16 to 0.94 ± 0.23 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover did not change, and total body adrenaline spillover increased significantly by about 30%. Clearances of noradrenaline and adrenaline were unchanged. 4. During lower body negative pressure at −40 mmHg, heart rate increased and pulse pressure decreased. Forearm vascular resistance increased by about 100%, and forearm noradrenaline spillover increased by 80%, from 0.73 ± 0.19 to 1.32 ± 0.36 pmol min−1 100 ml−1 (P<0.05). Total body noradrenaline spillover increased by 30%, and total body adrenaline spillover increased by about 50%. Clearances of both noradrenaline and adrenaline decreased. 5. The results are consistent with the view that selective deactivation of cardiopulmonary baroreceptors during low-intensity lower body negative pressure increases sympathoneural traffic to forearm skeletal muscle and increases adrenomedullary secretion without a concomitant generalized increase in sympathoneural outflows. Concurrent deactivation of cardiopulmonary and arterial baroreceptors during high-intensity lower body negative pressure evokes a more generalized increase in sympathoneural activity, accompanied by further increased adrenomedullary secretion and decreased plasma clearances of noradrenaline and adrenaline. The findings support differential increases in skeletal sympathoneural and adrenomedullary outflows during orthostasis, with more generalized sympathoneural responses to systemic hypotension.
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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 (October 1, 1993): 858–61. http://dx.doi.org/10.1139/y93-129.
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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, respectively). The presence of noradrenaline (0.1, 1, and 10 μM) in the medium increased the respiration rate of both kinds of adipocytes in a dose-dependent manner. However, the response was markedly reduced in adipocytes isolated from estradiol-treated rats. These results suggest that estradiol impairs the responsiveness of brown adipose tissue to the sympathetic nervous system. Three possible mechanisms are suggested as accounting for the observed decreased responsiveness to noradrenaline, i.e., a direct action of estradiol in brown adipocytes, a modulatory role of estradiol in the central control of the sympathetic discharge to brown adipose tissue, and the interference of catechoiestrogens with noradrenaline synthesis at the sympathetic terminals.Key words: brown adipocytes, estradiol, noradrenaline, oxygen consumption, sympathetic nervous system.
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Welberg, Leonie. "Noradrenaline arouses astrocytes." Nature Reviews Neuroscience 15, no. 8 (July 9, 2014): 495. http://dx.doi.org/10.1038/nrn3788.
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Loued-Khenissi, Leyla, and Kerstin Preuschoff. "Apathy and noradrenaline." Current Opinion in Neurology 28, no. 4 (August 2015): 344–50. http://dx.doi.org/10.1097/wco.0000000000000218.
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Beleslin, D. B., and M. Štrbac. "Noradrenaline-induced emesis." Neuropharmacology 26, no. 8 (August 1987): 1157–65. http://dx.doi.org/10.1016/0028-3908(87)90262-0.
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AYRAPETYANZ, M. G. "NORADRENALINE AND DOPAMINE." Behavioural Pharmacology 7, Supplement 1 (May 1996): 4. http://dx.doi.org/10.1097/00008877-199605001-00006.
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