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Journal articles on the topic 'Biosynthesis of rat adrenaline'

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1

Peltsch, Heather, Sandhya Khurana, Collin J. Byrne, et al. "Cardiac phenylethanolamine N-methyltransferase: localization and regulation of gene expression in the spontaneously hypertensive rat." Canadian Journal of Physiology and Pharmacology 94, no. 4 (2016): 363–72. http://dx.doi.org/10.1139/cjpp-2015-0303.

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Phenylethanolamine N-methyltransferase (PNMT) is the terminal enzyme in the catecholamine biosynthetic pathway responsible for adrenaline biosynthesis. Adrenaline is involved in the sympathetic control of blood pressure; it augments cardiac function by increasing stroke volume and cardiac output. Genetic mapping studies have linked the PNMT gene to hypertension. This study examined the expression of cardiac PNMT and changes in its transcriptional regulators in the spontaneously hypertensive (SHR) and wild type Wistar-Kyoto (WKY) rats. SHR exhibit elevated levels of corticosterone, and lower le
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2

Simonyi, Agnes, Bela Kanyicska, Tibor Szentendrei, and Marton I. K. Fekete. "Effect of chronic morphine treatment on the adrenaline biosynthesis in adrenals and brain regions of the rat." Biochemical Pharmacology 37, no. 4 (1988): 749–52. http://dx.doi.org/10.1016/0006-2952(88)90150-5.

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3

Shimbhu, Dawan, Kohichi Kojima, and Toshiharu Nagatsu. "A SENSITIVE ASSAY FOR NON-SPECIFIC N-METHYLTRANSFERASE ACTIVITY IN RAT TISSUES BY HIGH-PERFORMANCE LIQUID CHROMATOGRAPHY ELECTROCHEMICAL DETECTION." ASEAN Journal on Science and Technology for Development 19, no. 1 (2017): 63–68. http://dx.doi.org/10.29037/ajstd.318.

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Phenylethanolamine N-methyltransferase (PNMT) and non-specific N -methyltransferase (EC 2.1.1.28) catalyze the N-methylation of aromatic amines. PNMT is specific for phenylethanolamines such as noradrenaline (NA). and catalyzes the step in catecholamine biosynthesis, forming adrenaline (AD) from NA. PNMT activity is high in adrenal gland, whereas non-specific N-methyltransferase is distributed in various tissues such as the lungs. Borchardt et al. first reported a method to detect PNMT activity by high-performance liquid chromatography electrochemical detection (HPLC-EICD), which could demonst
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4

Shimojo, M., C. B. Whorwood та P. M. Stewart. "11β-Hydroxysteroid dehydrogenase in the rat adrenal". Journal of Molecular Endocrinology 17, № 2 (1996): 121–30. http://dx.doi.org/10.1677/jme.0.0170121.

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ABSTRACT 11β-Hydroxysteroid dehydrogenase (11β-HSD) catalyses the interconversion of biologically active cortisol to inactive cortisone in man, and corticosterone to 11-dehydrocorticosterone in rodents. As such, this enzyme has been shown to confer aldosterone-selectivity on the mineralocorticoid receptor and to modulate cortisol/corticosterone access to the glucocorticoid receptor (GR). Two kinetically distinct isoforms of this enzyme have been characterized in both rodents and man; a low-affinity NADP(H)-dependent enzyme (11β-HSD1) which predominantly acts as an oxo-reductase and, more recen
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5

Deng, Xinqi, Nan Jiang, Li Guo, et al. "Protective Effects and Metabolic Regulatory Mechanisms of Shenyan Fangshuai Recipe on Chronic Kidney Disease in Rats." Evidence-Based Complementary and Alternative Medicine 2020 (August 25, 2020): 1–13. http://dx.doi.org/10.1155/2020/5603243.

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Background. Chronic kidney disease (CKD) is one of the major causes of renal damage. Shenyan Fangshuai Recipe (SFR), a modified prescription of traditional medicine in China, showed potent effects in alleviating edema, proteinuria, and hematuria of CKD in clinical practices. In this study, we aimed to investigate scientific evidence-based efficacy as well as metabolic regulations of SFR in CKD treatment. Materials and Methods. The effect of SFR on CKD was observed in a rat model which is established with oral administration of adenine-ethambutol mixture for 21 days. Further, metabolites in ser
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Galan, Xavier, Julia Peinado-Onsurbe, Monique Q. Robert, Maria Soley, Miquel Llobera, and Ignasi Ramírez. "Acute regulation of hepatic lipase secretion by rat hepatocytes." Biochemistry and Cell Biology 80, no. 4 (2002): 467–74. http://dx.doi.org/10.1139/o02-136.

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Hepatic lipase is involved in cholesterol uptake by the liver. Although it is known that catecholamines are responsible for the daily variation of enzyme activity, the mechanisms involved are poorly understood. Rat hepatocytes incubated with adrenaline or other Ca2+-mobilizing hormones were used as an experimental model. Adrenaline reduced in a similar proportion the secretion of both hepatic lipase and albumin. The effect of adrenaline disappeared completely in cells exposed to cycloheximide. Adrenaline decreased incorporation of [35S]Met into cellular and secreted proteins, but it affected n
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7

Khurana, Sandhya, Sujeenthar Tharmalingam, Alyssa Murray, and T. C. Tai. "Epigenetic regulation of phenylethanolamine N‐methyltransferase: implications for adrenaline biosynthesis." FASEB Journal 34, S1 (2020): 1. http://dx.doi.org/10.1096/fasebj.2020.34.s1.04160.

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8

Costa, Vera M., Luísa M. Ferreira, Paula S. Branco, et al. "Characterization of adrenaline and adrenaline-GSH adduct transport in freshly isolated rat cardiomyocytes." Toxicology Letters 180 (October 2008): S99. http://dx.doi.org/10.1016/j.toxlet.2008.06.405.

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9

Napolitano, Gaetana, Daniela Barone, Sergio Di Meo, and Paola Venditti. "Adrenaline induces mitochondrial biogenesis in rat liver." Journal of Bioenergetics and Biomembranes 50, no. 1 (2017): 11–19. http://dx.doi.org/10.1007/s10863-017-9736-6.

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10

Nahar, Nurun, and Nargis Akhter. "Effect of carvedilol on adrenaline-induced changes in serum electrolytes in rat." Bangladesh Medical Research Council Bulletin 35, no. 3 (2010): 105–9. http://dx.doi.org/10.3329/bmrcb.v35i3.4116.

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Circulating catecholamine that is increased in early phase of myocardial infarction alters serum electrolyte levels which might predispose to serious ventricular arrhythmias. In this study the effect of pretreatment of carvedilol on adrenaline-induced changes in the serum electrolytes (Mg2+, K+, Ca2+, Na+) was evaluated in rats. Adrenaline was administered at a dose of 2 mg/kg body weight subcutaneously 2 injections 24 hours apart and serum electrolytes were estimated at 12 hours, 24 hours and 7 days after the 2nd injection of adrenaline. Adrenaline administration initially caused hypomagnesem
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11

GARCIA, Carolina, Tania C. PITHON-CURI, Maria DE LOURDES FIRMANO, Mariza PIRES DE MELO, Philip NEWSHOLME, and Rui CURI. "Effects of adrenaline on glucose and glutamine metabolism and superoxide production by rat neutrophils." Clinical Science 96, no. 6 (1999): 549–55. http://dx.doi.org/10.1042/cs0960549.

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Despite the large body of information on the role of corticosteroids in regulating lymphocyte and phagocyte function, the role of the hormone adrenaline in immunoregulation is an under-investigated topic. The present study has addressed the effects of adrenaline on the rates of utilization and oxidation of glucose and glutamine, the phagocytic capacity and the rate of superoxide production by rat neutrophils. Incubation of rat neutrophils in the presence of 50 µM adrenaline caused a marked elevation in glucose metabolism, an effect that could be blocked by propranolol. Adrenaline caused a part
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12

Abe, Nozomu, Hiroaki Toyama, Yutaka Ejima та ін. "α1-Adrenergic Receptor Blockade by Prazosin Synergistically Stabilizes Rat Peritoneal Mast Cells". BioMed Research International 2020 (13 травня 2020): 1–12. http://dx.doi.org/10.1155/2020/3214186.

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Background. Adrenaline quickly inhibits the release of histamine from mast cells. Besides β2-adrenergic receptors, several in vitro studies also indicate the involvement of α-adrenergic receptors in the process of exocytosis. Since exocytosis in mast cells can be detected electrophysiologically by the changes in the membrane capacitance (Cm), its continuous monitoring in the presence of drugs would determine their mast cell-stabilizing properties. Methods. Employing the whole-cell patch-clamp technique in rat peritoneal mast cells, we examined the effects of adrenaline on the degranulation of
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13

Sakata, S., and J. Iriuchijima. "Adrenomedullary origin of the hindquarter vasodilation during the transposition response of the rat." Canadian Journal of Physiology and Pharmacology 66, no. 1 (1988): 18–21. http://dx.doi.org/10.1139/y88-003.

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Transposing a rat from the home cage to a new cage produces a cardiovascular response (transposition response) characterized by an increase in hindquarter blood flow with unchanged systemic arterial pressure. Arterial blood samples were collected from rats before and during this response for radioenzymatic assay of catecholamines. During the transposition response, the concentration of adrenaline and noradrenaline in plasma increased about six- and two-fold, respectively. Ablation of the adrenal medulla prevented these changes in plasma catecholamine concentration. Constant i.v. infusion of ad
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14

Brindle, N. P., та J. A. Ontko. "α-adrenergic suppression of very-low-density-lipoprotein triacylglycerol secretion by isolated rat hepatocytes". Biochemical Journal 250, № 2 (1988): 363–68. http://dx.doi.org/10.1042/bj2500363.

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The effect of adrenaline on triacylglycerol synthesis and secretion was examined in isolated rat hepatocytes. Cells were incubated with 0.5 mM-[1-14C]oleate, and the accumulation of triacylglycerol and [14C]triacylglycerol was measured in the incubation medium. Triacylglycerol appearing in the medium was present in a form with properties similar to very-low-density lipoproteins. Triacylglycerol, [14C]triacylglycerol and [14C]phospholipid contents of hepatocytes were also determined. Addition of 10 microM-(-)adrenaline decreased accumulation of glycerolipid in the incubation medium and also dec
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15

Donsmark, Morten, Jozef Langfort, Cecilia Holm, Thorkil Ploug, and Henrik Galbo. "Regulation and role of hormone-sensitive lipase in rat skeletal muscle." Proceedings of the Nutrition Society 63, no. 2 (2004): 309–14. http://dx.doi.org/10.1079/pns2004359.

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Intramyocellular triacylglycerol (TG) is an important energy store, and the energy content of this depot is higher than the energy content of the muscle glycogen depot. It has recently been shown that the mobilization of fatty acids from this TG pool may be regulated by the neutral lipase hormone-sensitive lipase (HSL). This enzyme is known to be rate limiting for intracellular TG hydrolysis in adipose tissue. The presence of HSL has been demonstrated in all muscle fibre types by Western blotting of muscle fibres isolated by collagenase treatment or after freeze-drying. The content of HSL vari
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16

Block, K. P., B. W. Heywood, M. G. Buse, and A. E. Harper. "Activation of rat liver branched-chain 2-oxo acid dehydrogenase in vivo by glucagon and adrenaline." Biochemical Journal 232, no. 2 (1985): 593–97. http://dx.doi.org/10.1042/bj2320593.

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The activity of liver branched-chain 2-oxo acid dehydrogenase complex was measured in rats fed on low-protein diets and given adrenaline, glucagon, insulin or dibutyryl cyclic AMP in vivo. Administration of glucagon or adrenaline (200 micrograms/100 g body wt.) resulted in a 4-fold increase in the percentage of active complex. As with glucagon and adrenaline, treatment of rats with cyclic AMP (5 mg/100 g body wt.) resulted in marked activation of branched-chain 2-oxo acid dehydrogenase. Insulin administration (1 unit/100 g body wt.) also resulted in activation of enzyme; however, these effects
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17

Gardemann, A., H. Beck, and K. Jungermann. "Differential control of glycogenolysis and flow by arterial and portal acetylcholine in perfused rat liver." Biochemical Journal 271, no. 3 (1990): 599–604. http://dx.doi.org/10.1042/bj2710599.

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The effects of acetylcholine on glucose and lactate balance and on perfusion flow were studied in isolated rat livers perfused simultaneously via the hepatic artery (100 mmHg, 25-35% of flow) and the portal vein (10 mmHg, 75-65% of flow) with a Krebs-Henseleit bicarbonate buffer containing 5 mM-glucose, 2 mM-lactate and 0.2 mM-pyruvate. Arterial acetylcholine (10 microM sinusoidal concentration) caused an increase in glucose and lactate output and a slight decrease in arterial and portal flow. These effects were accompanied by an output of noradrenaline and adrenaline into the hepatic vein. Po
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18

Koh, Ho-Jin, Michael F. Hirshman, Huamei He, et al. "Adrenaline is a critical mediator of acute exercise-induced AMP-activated protein kinase activation in adipocytes." Biochemical Journal 403, no. 3 (2007): 473–81. http://dx.doi.org/10.1042/bj20061479.

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Exercise increases AMPK (AMP-activated protein kinase) activity in human and rat adipocytes, but the underlying molecular mechanisms and functional consequences of this activation are not known. Since adrenaline (epinephrine) concentrations increase with exercise, in the present study we hypothesized that adrenaline activates AMPK in adipocytes. We show that a single bout of exercise increases AMPKα1 and α2 activities and ACC (acetyl-CoA carboxylase) Ser79 phosphorylation in rat adipocytes. Similarly to exercise, adrenaline treatment in vivo increased AMPK activities and ACC phosphorylation. P
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19

Inglis, G. C., C. J. Kenyon, J. A. M. Hannah, J. M. C. Connell, and S. G. Ball. "Does dopamine regulate aldosterone secretion in the rat?" Clinical Science 73, no. 1 (1987): 93–97. http://dx.doi.org/10.1042/cs0730093.

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1. This study investigated the role of dopamine in the control of adrenal steroidogenesis. Adrenaline, noradrenaline and dopamine have been measured in plasma and in the adrenal zona glomerulosa and medulla of rats fed low, normal and high sodium diets and in zona glomerulosa tissue of rats with adrenal regeneration hypertension (ARH). 2. Adrenal concentrations (means ± se) of adrenaline, noradrenaline and dopamine in rats fed a normal diet were 1471 ± 335, 527 ± 75 and 51 ± 12 nmol/g in the medulla, and 66 ± 17, 18 ± 9 and 6 ± 1 nmol/g in the zona glomerulosa. The dopamine content of the zona
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20

Oyekan, A. O., and J. H. Botting. "The Influence of Adrenaline on Gender Difference in Adenosine Diphosphate-Induced Aggregation of Platelets in the Rat." Thrombosis and Haemostasis 60, no. 03 (1988): 481–85. http://dx.doi.org/10.1055/s-0038-1646995.

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SummaryThe role of adrenaline on the inhibitory effects of physiological levels of oestradiol on ADP-induced intravascular aggregation has been studied. Platelets from pro-oestrous female rats aggregated less than those from dioestrous and male rats. Following adrenalectomy, there was no longer any difference(s) in the aggregability of the platelets to ADP in any of the rats. Adrenaline infusion (20 mg kg−1 hr−1) restored platelet aggregation to preadrenalectomy levels in pro-oestrous rate. Measurement of spontaneous fibrinolytic activity of the plasma showed highest value in pro-oestrous rats
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21

Pelto-Huikko, M., T. Salminen, and A. Hervonen. "Localization of enkephalins in adrenaline cells and the nerves innervating adrenaline cells in rat adrenal medulla." Histochemistry 82, no. 4 (1985): 377–83. http://dx.doi.org/10.1007/bf00494067.

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22

Layland, J., I. S. Young, and J. D. Altringham. "The effects of adrenaline on the work- and power-generating capacity of rat papillary muscle in vitro." Journal of Experimental Biology 200, no. 3 (1997): 503–9. http://dx.doi.org/10.1242/jeb.200.3.503.

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The work loop technique was used to examine the effects of adrenaline on the mechanics of cardiac muscle contraction in vitro. The length for maximum active force (Lmax) and net work production (Lopt) for rat papillary muscles was determined under control conditions (without adrenaline). The concentration of adrenaline producing the maximum inotropic effect was determined. This concentration was used in the remainder of the experiments. Sinusoidal strain cycles about Lopt were performed over a physiologically relevant range of cycle frequencies (4-11 Hz). Maximum work and the frequency for max
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Bertrand, G., M. Nenquin та J. C. Henquin. "Comparison of the inhibition of insulin release by activation of adenosine and α2-adrenergic receptors in rat β-cells". Biochemical Journal 259, № 1 (1989): 223–28. http://dx.doi.org/10.1042/bj2590223.

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Rat islets were used to compare the mechanisms whereby adenosine and adrenaline inhibit insulin release. Adenosine (1 microM-2.5 mM) and its analogue N6(-)-phenylisopropyladenosine (L-PIA) (1 nM-10 microM) caused a concentration-dependent but incomplete (45-60%) inhibition of glucose-stimulated release. L-PIA was more potent than D-PIA [the N6(+) analogue], but much less than adrenaline, which caused nearly complete inhibition (85% at 0.1 microM). 8-Phenyltheophylline prevented the inhibitory effect of L-PIA and 50 microM-adenosine, but not that of 500 microM-adenosine or of adrenaline. In con
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24

Helman, J., G. S. Roth, and B. J. Baum. "Adrenergic-agonist-induced Ca2+ fluxes in rat parotid cells are not Na+-dependent." Biochemical Journal 230, no. 2 (1985): 313–20. http://dx.doi.org/10.1042/bj2300313.

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We investigated the hypothesis that extracellular Na+ is required for the rapid mobilization of Ca2+ by rat parotid cells after adrenergic stimulation. When Na+ salts in the media were osmotically replaced with either choline chloride (+atropine) or sucrose, efflux of 45Ca2+ from preloaded cells, caused by 10 microM-(-)-adrenaline, was unchanged. Similarly adrenaline stimulated 45Ca2+ uptake into cells under nonsteady-state conditions in the presence or absence of Na+. Monensin, a Na+ ionophore, was able to elicit a modest increase in 45Ca2+ efflux, compared with controls. Studies of net 45Ca2
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25

Ainscow, Edward K., and Martin D. Brand. "The responses of rat hepatocytes to glucagon and adrenaline." European Journal of Biochemistry 265, no. 3 (2001): 1043–55. http://dx.doi.org/10.1046/j.1432-1327.1999.00820.x.

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26

FRANCH, Jesper, Rune ASLESEN, and Jørgen JENSEN. "Regulation of glycogen synthesis in rat skeletal muscle after glycogen-depleting contractile activity: effects of adrenaline on glycogen synthesis and activation of glycogen synthase and glycogen phosphorylase." Biochemical Journal 344, no. 1 (1999): 231–35. http://dx.doi.org/10.1042/bj3440231.

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We investigated the effects of insulin and adrenaline on the rate of glycogen synthesis in skeletal muscles after electrical stimulation in vitro. The contractile activity decreased the glycogen concentration by 62%. After contractile activity, the glycogen stores were fully replenished at a constant and high rate for 3 h when 10 m-i.u./ml insulin was present. In the absence of insulin, only 65% of the initial glycogen stores was replenished. Adrenaline decreased insulin-stimulated glycogen synthesis. Surprisingly, adrenaline did not inhibit glycogen synthesis stimulated by glycogen-depleting
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27

Pal, Palash Kumar, Swaimanti Sarkar, Sanatan Mishra, Sreya Chattopadhyay, Aindrila Chattopadhyay та Debasish Bandyopadhyay. "Amelioration of adrenaline induced oxidative gastrointestinal damages in rat by melatonin through SIRT1-NFκB and PGC1α-AMPKα cascades". Melatonin Research 3, № 4 (2020): 482–502. http://dx.doi.org/10.32794/mr11250074.

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Adrenaline at high pharmacological doses may lead to oxidative damages in diverse organs including gut. In this study, we attempt to elucidate the potentially protective effects of melatonin on gastrointestinal (GI) tissue damages induced by adrenaline. Rats were injected (s.c.) with different doses (0.125, 0.25 and 0.50 mg/kg) of adrenaline bitartrate (AD) for 15 days with or without melatonin (2.5, 5 and 10 mg/kg; orally). The results showed that adrenaline caused massive histological and ultra-structural GI injuries and melatonin (20 mg/kg) effectively protected these injuries. The protecti
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28

NORTHEMANN, WOLFGANG, MICHAEL HEISIG, DIETER KUNZ та ін. "Biosynthesis of rat α2-macroglobulin". Biochemical Society Transactions 13, № 2 (1985): 285–88. http://dx.doi.org/10.1042/bst0130285.

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29

Sanin, V. V., A. I. Yakovets, K. V. Rozova, et al. "EFFECT OF N-ACETYLCARNOSINE CONTAINED EYE DROP ON CATECHOLAMINE-INDUCED MORPHOFUNCTIONAL DAMAGE IN RAT RETINA." Fiziolohichnyĭ zhurnal 66, no. 4 (2020): 64–71. http://dx.doi.org/10.15407/fz66.04.064.

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The effects of N-acetylcarnosine (NAC)-contained eye drop ‘Clarastil’ on a model of adrenaline-induced high intraocular pressure (IOP) in Wistar rats were studied. The retina ultrastructure and markers of oxidative stress have been studied. NAC was found to have no significant effect on edema in the retinal ultrastructure, did not reduce endothelial thickening and histogemic barrier, and accordingly did not affect the value of IOP after prolonged adrenaline administration. However, the introduction of the eye drop prevented the swelling of the mitochondria, the formation of vacuolated crystals
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30

Pal, Palash Kumar, Bharati Bhattacharjee, Arnab Kumar Ghosh, Aindrila Chattopadhyay, and Debasish Bandyopadhyay. "Adrenaline induced disruption of endogenous melatoninergic system, antioxidant and inflammatory responses in the gastrointestinal tissues of male Wistar rat: an in vitro study." Melatonin Research 1, no. 1 (2018): 109–31. http://dx.doi.org/10.32794/mr11250007.

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The current study aimed to demonstrate the potentially adverse effects of adrenaline, an endogenous stressor, on the melatonergic system, oxidative status, antioxidative responses and inflammatory markers in different parts of gastrointestinal tract of Wistar rat. These included stomach, duodenum and colon and they were incubated with different concentrations (2.5, 5.0 and 10.0 µg/mL) of adrenaline for 1h, respectively. The levels of melatonin, gene expressions of arylalkylamine N-acetyltransferase (AANAT) and melatonin receptor 1 (MT1) as well as other stress-induced parameters including NF-k
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Poggioli, J., J. P. Mauger, and M. Claret. "Effect of cyclic AMP-dependent hormones and Ca2+-mobilizing hormones on the Ca2+ influx and polyphosphoinositide metabolism in isolated rat hepatocytes." Biochemical Journal 235, no. 3 (1986): 663–69. http://dx.doi.org/10.1042/bj2350663.

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The effect of the interaction between the Ca2+-mobilizing hormone adrenaline, used as alpha-adrenergic agonist, and cyclic AMP-dependent hormones, including beta-adrenergic agonists and glucagon, on the initial 45Ca2+ uptake rate and polyphosphoinositide metabolism were investigated in isolated rat hepatocytes. Each hormone alone increased the initial 45Ca2+ uptake rate. When adrenaline was added without inhibitor, it induced a rise in the initial 45Ca2+ uptake rate larger than the sum of the rises elicited by its alpha and beta components singly. Similarly, when adrenaline was used as an alph
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32

Wlllerth, M., and J. A. Thornhill. "The effects of endogenous opioids on tension development of isolated, electrically stimulated rat atria." Canadian Journal of Physiology and Pharmacology 65, no. 6 (1987): 1227–33. http://dx.doi.org/10.1139/y87-194.

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The possible inotropic effects of all three classes of endogenous opioids were tested alone or in combination with noradrenaline, adrenaline, or carbachol on electrically stimulated atria isolated from male Sprague–Dawley rats. Noradrenaline (6.0 and 12 μM) and adrenaline (4.0 and 8.0 μM) injections caused marked but transient (5 min) dose-related increases in atrial tension compared with preinjection control values, whereas carbachol (0.14 and 1.4 μM) caused a more potent and prolonged (over 15 min) dose-related decrease in atrial tension development. Adrenal enkephalins (0.3–4.0 μM) of methi
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33

Kilgour, E., and R. G. Vernon. "Catecholamine activation of pyruvate dehydrogenase in white adipose tissue of the rat in vivo." Biochemical Journal 241, no. 2 (1987): 415–19. http://dx.doi.org/10.1042/bj2410415.

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Intraperitoneal injections of noradrenaline or adrenaline into rats increased the proportion of pyruvate dehydrogenase in the active state in white adipose tissue; this effect of catecholamines was also apparent in streptozotocin-diabetic rats, showing that it was not due to an increase in serum insulin concentration. The catecholamine-induced increase in pyruvate dehydrogenase of white adipose tissue in vivo was completely blocked by prior injection of either the beta-antagonist propranolol or the alpha 1-antagonist prazosin. Cervical dislocation of conscious rats increased pyruvate dehydroge
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34

Jensen, Kjell Briseid, and Reidar Bredo Sund. "The Inhibitory Action of Adrenaline on the Isolated Rat Uterus." Acta Pharmacologica et Toxicologica 17, no. 2 (2009): 173–81. http://dx.doi.org/10.1111/j.1600-0773.1960.tb01241.x.

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35

Jensen, Kjell Briseid, and Anne Marie Venneröd. "Determination of Adrenaline on the Isolated Serotonin-Stimulated Rat Uterus." Acta Pharmacologica et Toxicologica 18, no. 1 (2009): 80–88. http://dx.doi.org/10.1111/j.1600-0773.1961.tb00315.x.

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36

Bouryi, Vitali A., and David I. Lewis. "Adrenaline modulates multiple conductances in rat vagal motoneurones in vitro." Neuroreport 12, no. 8 (2001): 1709–13. http://dx.doi.org/10.1097/00001756-200106130-00038.

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37

Kujacic, Mirjana, Lars O. Hansson, and Arvid Carlsson. "Acute dopaminergic influence on plasma adrenaline levels in the rat." European Journal of Pharmacology 273, no. 3 (1995): 247–57. http://dx.doi.org/10.1016/0014-2999(94)00699-8.

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38

Quintana, I., M. Grau, F. Moreno, C. Soler, I. Ramírez, and M. Soley. "The early stimulation of glycolysis by epidermal growth factor in isolated rat hepatocytes is secondary to the glycogenolytic effect." Biochemical Journal 308, no. 3 (1995): 889–94. http://dx.doi.org/10.1042/bj3080889.

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We have studied the relationship between the effect of epidermal growth factor (EGF) on glycogen metabolism and its effect on glycolysis, in rat hepatocyte suspensions. Although 10 nM glucagon or 10 microM adrenaline increased glycogen degradation by more than 120%, 10 nM EGF increased glycogenolysis by less than 20% in hepatocytes incubated in glucose-free medium. Both glucagon and adrenaline increased phosphorylase a activity by more than 130%; EGF increased this activity by about 30%. Under basal conditions, 65% of the glucosyl residues were released as free glucose and about 30% ended up a
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39

Hildebrandt, E. F., D. B. Buxton, and M. S. Olson. "Acute regulation of the branched-chain 2-oxo acid dehydrogenase complex by adrenaline and glucagon in the perfused rat heart." Biochemical Journal 250, no. 3 (1988): 835–41. http://dx.doi.org/10.1042/bj2500835.

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Rates of transamination and decarboxylation of [1-14C]leucine at a physiological concentration (0.1 mM) were measured in the perfused rat heart. In hearts from fasted rats, metabolic flux through the branched-chain 2-oxo acid dehydrogenase reaction was low initially, but increased gradually during the perfusion period. The increase in 14CO2 production was accompanied by an increase in the amount of active branched-chain 2-oxo acid dehydrogenase complex present in the tissue. In hearts from rats fed ad libitum, extractable branched-chain dehydrogenase activity was low initially, but increased r
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Kuchmenko, O. B., D. M. Petukhov, I. N. Yevstratova, L. S. Mkhitaryan та G. V. Donchenko. "Ефект попередників і модуляторів біосинтезу убіхінону на вміст і функціонування убіхінону та оксидативний статус у серці при введенні адреналіну". Visnyk of Dnipropetrovsk University. Biology, medicine 2, № 1 (2011): 68–74. http://dx.doi.org/10.15421/021111.

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Preventive and/or subsequent application of precursors and modulators complexes of ubiquinone biosynthesis under the adrenaline treatment reduces free-radical lipid and protein peroxidation intensity, but increases superoxide dismutase activity and improves activities of the mitochondrial electron-transport chain complexes. EPM and EPMD complexes can be effective anti-hypoxic remedies that promote normalization of the energy metabolism in ischemic heart.
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Burns, G., B. L. Brown, and P. R. M. Dobson. "Diurnal variation in the effect of potassium depolarization on vasoactive intestinal polypeptide release from rat hypothalamus: a possible role for adrenaline." Journal of Endocrinology 116, no. 3 (1988): 335–41. http://dx.doi.org/10.1677/joe.0.1160335.

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ABSTRACT We have previously reported a lack of effect of a depolarizing concentration of K+ on the release of vasoactive intestinal polypeptide (VIP) from the perifused rat hypothalamus, and suggested that this was due to the presence of an endogenous inhibitor of the release of VIP. In this study we report that the VIP response to K+ was restored if the hypothalami were obtained from animals killed during the dark phase of the light–dark cycle. Adrenaline blocked the K+-stimulated release of VIP when used at a concentration of 0·1 μmol/l; however, at a higher concentration (10 μmol/l) adrenal
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Higuchi, T., H. Negoro, and J. Arita. "Reduced responses of prolactin and catecholamine to stress in the lactating rat." Journal of Endocrinology 122, no. 2 (1989): 495–98. http://dx.doi.org/10.1677/joe.0.1220495.

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ABSTRACT Prolactin, GH, TSH, adrenaline and noradrenaline responses to the stress of immobilization were compared between lactating and non-lactating dioestrous rats. The concentrations of GH in plasma were reduced to a similar degree by the immobilization of lactating and non-lactating rats, and TSH levels were unchanged in both groups. The increases in plasma concentrations of adrenaline and noradrenaline induced by stress were significantly smaller in lactating than in non-lactating rats. Immobilization caused a marked increase in prolactin levels in the plasma of non-lactating rats but no
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CLARK, Andrew D. H., Eugene J. BARRETT, Stephen RATTIGAN, Michelle G. WALLIS, and Michael G. CLARK. "Insulin stimulates laser Doppler signal by rat muscle in vivo, consistent with nutritive flow recruitment." Clinical Science 100, no. 3 (2001): 283–90. http://dx.doi.org/10.1042/cs1000283.

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Insulin-mediated increases in limb blood flow are thought to enhance glucose uptake by skeletal muscle. Using the perfused rat hindlimb, we report that macro laser Doppler flowmetry (LDF) probes positioned on the surface of muscle detect changes in muscle capillary (nutritive) flow. With this as background, we examined the effects of insulin and adrenaline (epinephrine), which are both known to increase total leg blood flow, on the LDF signals from scanning and stationary probes on the muscle surface in vivo. The aim is to assess the relationship between capillary recruitment, total limb blood
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Kalén, A., E. L. Appelkvist, G. Dallner, Bertil Andersson, and Hans-Erik Åkerlund. "Biosynthesis of Ubiquinone in Rat Liver." Acta Chemica Scandinavica 41b (1987): 70–72. http://dx.doi.org/10.3891/acta.chem.scand.41b-0070.

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Appelkvist, Eeva-Liisa, Ole Hammerich, Vernon D. Parker, Bertil Andersson, and Hans-Erik Åkerlund. "Dolichol Biosynthesis in Rat Liver Peroxisomes." Acta Chemica Scandinavica 41b (1987): 73–75. http://dx.doi.org/10.3891/acta.chem.scand.41b-0073.

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McCOLL, K. E. L., F. M. BOND, G. G. THOMPSON, and M. R. MOORE. "Haem biosynthesis in the Gunn rat." Biochemical Society Transactions 14, no. 5 (1986): 921–22. http://dx.doi.org/10.1042/bst0140921.

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Gomez-Sanchez, Celso E., Ming Yi Zhou, Eduardo N. Cozza, Hiroyuki Morita, Mark F. Foecking, and Elise P. Gomez-Sanchez. "Aldosterone Biosynthesis in the Rat Brain1." Endocrinology 138, no. 8 (1997): 3369–73. http://dx.doi.org/10.1210/endo.138.8.5326.

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Tekle, Michael, Magnus Bentinger, Tomas Nordman, Eeva-Liisa Appelkvist, Tadeusz Chojnacki, and Jerker M. Olsson. "Ubiquinone Biosynthesis in Rat Liver Peroxisomes." Biochemical and Biophysical Research Communications 291, no. 5 (2002): 1128–33. http://dx.doi.org/10.1006/bbrc.2002.6537.

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Tsuchiya, Yugo, Fiona C. Denison, Richard B. Heath, David Carling, and David Saggerson. "5′-AMP-activated protein kinase is inactivated by adrenergic signalling in adult cardiac myocytes." Bioscience Reports 32, no. 2 (2011): 197–209. http://dx.doi.org/10.1042/bsr20110076.

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In adult rat cardiac myocytes adrenaline decreased AMPK (AMP-activated protein kinase) activity with a half-time of approximately 4 min, decreased phosphorylation of AMPK (α-Thr172) and decreased phosphorylation of ACC (acetyl-CoA carboxylase). Inactivation of AMPK by adrenaline was through both α1- and β-ARs (adrenergic receptors), but did not involve cAMP or calcium signalling, was not blocked by the PKC (protein kinase C) inhibitor BIM I (bisindoylmaleimide I), by the ERK (extracellular-signal-regulated kinase) cascade inhibitor U0126 or by PTX (pertussis toxin). Adrenaline caused no measur
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Mishra, Sanatan, Aindrila Chattopadhyay, Shamreen Naaz, Arnab K. Ghosh, Asish Ranjan Das, and Debasish Bandyopadhyay. "Oleic acid ameliorates adrenaline induced dysfunction of rat heart mitochondria by binding with adrenaline: An isothermal titration calorimetry study." Life Sciences 218 (February 2019): 96–111. http://dx.doi.org/10.1016/j.lfs.2018.12.035.

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