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Journal articles on the topic 'Adrenalina - Receptores'

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Published: 4 June 2021

Last updated: 1 February 2022

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1

Delgado Prado, Emma Daniela, Alejandro Córdova Izquierdo, Miguel Ángel García Díaz, et al. "Actores de la cadena productiva que deben participar para prevenir el uso de clembuterol en la engorda del ganado bovino en México." Revista Biológico Agropecuaria Tuxpan 5, no. 1 (2017): 97–104. http://dx.doi.org/10.47808/revistabioagro.v5i1.98.

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El clembuterol, Químicamente se describe como polvo blanco, anhidro, muy soluble en agua y altamente estable a temperatura ambiente, su punto de fusión es de 174 a 175.5 ºC. También es un derivado sintético perteneciente a una clase de medicamentos análogos fisiológicamente a la adrenalina, tiene la capacidad de interactuar con receptores adrenérgicos, generalmente del tipo ß2 (β agonista), es uno de los modificadores metabólicos más conocido en el área de producción de carne, debido al alto grado residual que deja esta sustancia en los tejidos comestibles y sus posibles repercusiones en la sa

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2

Meyerholz, H. H., A. Gardemann, and K. Jungermann. "Control of glycogenolysis and blood flow by arterial and portal adrenaline in perfused liver." Biochemical Journal 275, no. 3 (1991): 609–16. http://dx.doi.org/10.1042/bj2750609.

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In isolated liver from fed rats, simultaneously single-pass-perfused via both the hepatic artery (80 mmHg, 30-35% flow) and the portal vein (10 mmHg, 70-65% flow), adrenaline was infused either singly or jointly via the hepatic artery or the portal vein in the absence or presence of the alpha 1-blocker prazosin and the beta 2-blocker butoxamine. It was found that: (1) arterial adrenaline caused increases in glucose and lactate output which were slower in onset, smaller in peak height but longer in duration than did portal adrenaline; (2) arterial adrenaline elicited a much more pronounced decr

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3

Schrader, Thomas, and Michael Herm. "Towards synthetic adrenaline receptors." Materials Science and Engineering: C 18, no. 1-2 (2001): 147–55. http://dx.doi.org/10.1016/s0928-4931(01)00383-6.

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4

Herm, Michael, and Thomas Schrader. "Towards Synthetic Adrenaline Receptors." Chemistry - A European Journal 6, no. 1 (2000): 47–53. http://dx.doi.org/10.1002/(sici)1521-3765(20000103)6:1<47::aid-chem47>3.0.co;2-i.

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5

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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6

Herm, Michael, Oliver Molt, and Thomas Schrader. "Towards Synthetic Adrenaline Receptors—Shape-Selective Adrenaline Recognition in Water." Angewandte Chemie International Edition 40, no. 17 (2001): 3148–51. http://dx.doi.org/10.1002/1521-3773(20010903)40:17<3148::aid-anie3148>3.0.co;2-s.

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7

Herm, Michael, Oliver Molt, and Thomas Schrader. "Towards Synthetic Adrenaline Receptors—Shape-Selective Adrenaline Recognition in Water." Chemistry - A European Journal 8, no. 6 (2002): 1485–99. http://dx.doi.org/10.1002/1521-3765(20020315)8:6<1485::aid-chem1485>3.0.co;2-h.

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8

Herm, Michael, and Thomas Schrader. "Synthetic Adrenaline Receptors Based on Bisphosphonates." Phosphorus, Sulfur, and Silicon and the Related Elements 144, no. 1 (1999): 749–52. http://dx.doi.org/10.1080/10426509908546353.

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9

Convents, A., J. P. De Backer, C. André та G. Vauquelin. "Desensitization of α2-adrenergic receptors in NG 108 15 cells by (–)-adrenaline and phorbol 12-myristate 13-acetate". Biochemical Journal 262, № 1 (1989): 245–51. http://dx.doi.org/10.1042/bj2620245.

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alpha 2-Adrenergic receptors on NG 108 15 cell membranes were identified by [3H]rauwolscine binding: Bmax. = 661 +/- 81 fmol/mg of protein, Kd = 6.9 +/- 2.5 nM (mean +/- S.E.M., n = 6). On intact cells, stimulation of these receptors by (-)-adrenaline inhibited the prostaglandin-E1-stimulated adenylate cyclase activity by about 60%. The effect of (-)-adrenaline was pertussis-toxin-sensitive, indicating the involvement of an inhibitory G protein. (-)-Adrenaline/[3H]rauwolscine competition-binding experiments revealed that only 50% of the alpha 2 receptors were coupled to G proteins (i.e. displa

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10

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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11

Porta, S., H. M. H. Hofmann, U. Ertl, et al. "Preventive action of phentolamine on adrenaline induced blood glucose elevation in humans." Acta Endocrinologica 117, no. 2 (1988): 166–72. http://dx.doi.org/10.1530/acta.0.1170166.

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Abstract. A comparison of the action of adrenaline infusion and a combined adrenaline + alpha blocker (phentolamine, Regitine®) infusion on blood glucose (BG), plasma immunoreactive insulin (IRI), BG/IRI ratio, C-peptide, and plasma cortisol levels was made in healthy young human subjects. The purpose of the experiment was to check, whether alpha block could abolish adrenaline-induced enhancement of blood glucose levels. The results show that during enhanced adrenaline levels, the use of regitine could indeed normalize blood glucose levels, not so much by increasing the IRI secretion, but by d

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12

Steen, Vidar M., Holm Holmsen та Grethe Aarbakke. "The Platelet-Stimulating Effect of Adrenaline Through α2-Adrenergic Receptors Requires Simultaneous Activation by a True Stimulatory Platelet Agonist". Thrombosis and Haemostasis 70, № 03 (1993): 506–13. http://dx.doi.org/10.1055/s-0038-1649614.

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SummaryThe stimulating effect of adrenaline on human platelet phospholipase C (PLC) activation and responses in vitro (shape change, aggregation and dense granule secretion) was investigated with respect to its dependence on exogenously added agonists. All experiments were performed with human gel-filtered platelets pretreated with acetylsalicylic acid to prevent endogenous stimulation by the arachidonate pathway. (1) Preliminary experiments demonstrated the presence of trace amounts of extracellular ADP (0.05-0.58 μM) in non-stimulated platelet suspensions; ADP was effectively converted to AT

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13

Green, Rachel J., and D. N. Baron. "Lack of effect of acute ethanol consumption on active cation fluxes of leucocytes and erythrocytes in healthy humans." Clinical Science 73, no. 4 (1987): 387–93. http://dx.doi.org/10.1042/cs0730387.

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1. Acute ethanol consumption in human volunteers did not appear to alter active cation fluxes by Na+,K+-ATPase, or intracellular electrolyte concentrations, in peripheral leucocytes or erythrocytes. 2. Urinary electrolyte excretion was decreased after ethanol consumption, compared with controls. 3. Neither plasma glucose nor serum insulin was altered by ethanol. 4. After ethanol consumption there was an elevation of endogenous plasma adrenaline levels. This was accompanied by a leucocytosis, which could be attributed to a raised neutrophil count. 5. The raised adrenaline levels were not associ

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14

Eldadah, Basil A., Sandra L. Pechnik, Courtney S. Holmes, Jeffrey P. Moak, Ahmed M. Saleem, and David S. Goldstein. "Failure of propranolol to prevent tilt-evoked systemic vasodilatation, adrenaline release and neurocardiogenic syncope." Clinical Science 111, no. 3 (2006): 209–16. http://dx.doi.org/10.1042/cs20060017.

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In patients with neurocardiogenic syncope, head-up tilt often evokes acute loss of consciousness accompanied by vasodilatation, increased plasma adrenaline and systemic hypotension. Since hypotension increases adrenaline levels and adrenaline can produce skeletal muscle vasodilatation by activating β2 receptors, adrenaline might induce a positive feedback loop precipitating circulatory collapse. We hypothesized that propranolol, a non-selective β-blocker, would prevent adrenaline-induced vasodilatation and thereby prevent syncope. Eight subjects with recurrent neurocardiogenic syncope and prev

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15

Lalau Keraly, C., J. D. Vickers, R. L. Kinlough-Rathbone, and J. F. Mustard. "Involvement of phosphoinositide metabolism in potentiation by adrenaline of ADP-induced aggregation of rabbit platelets." Biochemical Journal 242, no. 3 (1987): 841–47. http://dx.doi.org/10.1042/bj2420841.

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Changes in phosphoinositide metabolism were examined in washed rabbit platelets stimulated with 0.5 microM-ADP, 50 microM-adrenaline, or ADP and adrenaline in combination. Adrenaline does not stimulate platelet aggregation when used alone, but does potentiate aggregation stimulated by ADP. In platelets prelabelled with [32P]Pi and [3H]glycerol, adrenaline was found to potentiate the ADP-induced changes in platelet phospholipids, causing larger increases in the amount and labelling of phosphatidylinositol 4-phosphate (PIP) and phosphatidic acid than was observed with ADP alone. The combination

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16

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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17

Ehrhart-Bornstein, M., S. R. Bornstein, W. H. Trzeclak, et al. "ADRENALINE STIMULATES CHOLESTEROL SIDE-CHAIN CLEAVAGE CYTOCHROME P450 mRNA ACCUMULATION IN BOVINE ADRENOCORTICAL CELLS." Journal of Endocrinology 131, no. 2 (1991): R5—R8. http://dx.doi.org/10.1677/joe.0.131r005.

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ABSTRACT The effect of adrenaline on the accumulation of mRNA encoding cholesterol side-chain cleavage cytochrome P450 (P450scc) and cortisol secretion was studied in bovine adrenocortical cells in primary culture. Treatment of cultured cells with adrenaline resulted in a 2-fold increase in mRNA encoding P-450scc, as revealed by Northern blot analysis. Under these conditions the maximal stimulation with ACTH resulted in a 6-fold accumulation of mRNA encoding P450scc. The effect of adrenaline on the expression of P450scc was abolished by the ß-blocker propranolol, while propranolol had no effec

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18

Lanza, François, and Jean-Pierre Cazenave. "Studies of Alpha2-Adrenergic Receptors of Intact and Functional Washed Human Platelets by Binding of 3H-Dihydroergocryptine and 3H-Yohimbine-Correlation of 3H-Yohimbine Binding with the Potentiation by Adrenaline of ADP-Induced Aggregation." Thrombosis and Haemostasis 54, no. 02 (1985): 402–8. http://dx.doi.org/10.1055/s-0038-1657749.

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SummaryThe binding of 3H-dihydroergocryptine and 3H-yohimbine to intact, discoid, functional, washed human platelets resuspended in Tyrode’s buffer containing Ca2+, Mg2+, human albumin and apyrase, was studied at 37° C. The binding of 3H-dihydroergocryptine was rapid, reversible and saturable (KD = 19.3 ± 4.2 nM, Bmax = 2590 ± 670 sites per platelet). The results were difficult to interpret because the bound ligand was not easily dissociated. In contrast, 3H-yohimbine bound in a rapid, reversible and saturable fashion to one class of sites (KD = 8.1 ± 1 nM, Bmax = 395 ± 35 sites/platelet) with

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19

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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20

Inyang, A. L., and D. T. Okpako. "Responses of the isolated rectum of the rainbow lizard (Agama agama) to sympathomimetics." Canadian Journal of Physiology and Pharmacology 67, no. 1 (1989): 68–71. http://dx.doi.org/10.1139/y89-011.

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The relaxant effects of isoprenaline, noradrenaline, and adrenaline on the isolated rectum of the rainbow lizard (Agama agama) were studied. Responses were measured as a reduction of carbachol-induced contractions for each sympathomimetic agent. Isoprenaline, adrenaline, noradrenaline produced a dose-dependent relaxation of this preparation and the order of potency was as given. The pD2 value of 8.15 ± 1.88 obtained for isoprenaline was significantly different (p < 0.05) from those for adrenaline (5.80 ± 0.90) and noradrenaline (5.25 ± 1.18). H35/25, propranolol, and practolol competitively

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21

May, Clive N., Catherine J. Whitehead, Kirsten E. Heslop, and Christopher J. Mathias. "Evidence that intravenous morphine stimulates central opiate receptors to increase sympatho-adrenal outflow and cause hypertension in conscious rabbits." Clinical Science 76, no. 4 (1989): 431–37. http://dx.doi.org/10.1042/cs0760431.

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1. In conscious rabbits, intravenous morphine caused hypertension, bradycardia, hyperglycaemia and increased plasma adrenaline and noradrenaline. These effects were prevented by ganglionic blockade with pentolinium. 2. The cardiovascular responses to morphine were not altered by pretreatment with a vasopressin V1-receptor antagonist. 3. After bilateral adrenalectomy morphine caused a similar rise in noradrenaline but no increase in adrenaline. The rise in blood pressure was attenuated and the hyperglycaemia was abolished. 4. Adrenaline infused intravenously to mimic the levels that occurred af

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22

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

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

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23

Ramos, Inés, Susana Cisint, Claudia A. Crespo, Marcela F. Medina, and Silvia N. Fernández. "Involvement of catecholamines in the regulation of oocyte maturation in frogs." Zygote 10, no. 3 (2002): 271–81. http://dx.doi.org/10.1017/s0967199402002356.

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The present study investigates the role of catecholamines in the regulation of Bufo arenarum oocyte maturation. The metabolic changes in the oxidation of carbohydrates and the meiotic resumption evinced by the germinal vesicle breakdown were used as indicators of cytoplasmic and nuclear maturation, respectively. The results obtained suggest that noradrenaline (norepinephrine) could be one of the factors responsible for the metabolic behaviour that characterises cytoplasmically immature oocytes. The use of adrenaline (epinephrine), on the other hand, induced a metabolic change which made oocyte

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Montpetit, C. J., and S. F. Perry. "Neuronal control of catecholamine secretion from chromaffin cells in the rainbow trout (Oncorhynchus mykiss)." Journal of Experimental Biology 202, no. 15 (1999): 2059–69. http://dx.doi.org/10.1242/jeb.202.15.2059.

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The goal of the present investigation was to assess the relative involvement of nicotinic and muscarinic cholinergic receptors in the neuronal control of catecholamine secretion from the chromaffin tissue of rainbow trout (Oncorhynchus mykiss). This was accomplished by first developing and validating a nerve-stimulating technique able specifically to activate the nerve fibres innervating the chromaffin cells in order to elicit secretion of catecholamines. Using an in situ saline-perfused posterior cardinal vein preparation, it was demonstrated that whole-body field stimulation caused specific

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Hill, C. E., A. P. Dawson, and J. S. Pryor. "Evidence for adrenergic control of transcellular calcium distribution in liver." Biochemical Journal 230, no. 3 (1985): 733–37. http://dx.doi.org/10.1042/bj2300733.

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Free Ca2+ concentration and 45Ca flux were measured in the perfusate and bile of the perfused rat liver. With a perfusate Ca2+ concentration of 1 mM, the bile concentration was 0.35 mM. The ratio of 45Ca in bile to that in blood increased from 0.3 to 0.6 over 90 min of perfusion. Both verapamil and adrenaline (via α-adrenergic receptors) increased the 45Ca bile/perfusate ratio to 0.8. Adrenaline infusion increased the bile Ca2+ concentration to 0.8 mM. This decreased to 0.35 mM after the infusion was stopped.

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Mansur, Cristina, Leonora Mansur, João Mansur, Maria Teresa Feital, Itabyba Martins Miranda Chaves, and Aloísio Couri Gamonal. "Aprimoramentos no transplante de cabelo com laser de CO2: apresentação de três casos clínicos." Anais Brasileiros de Dermatologia 79, no. 2 (2004): 199–204. http://dx.doi.org/10.1590/s0365-05962004000200008.

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Os autores apresentam três casos de transplante de cabelo em que foram feitas incisões receptoras mistas: orifício com vaporização com laser de CO2 nos quais se adicionou uma incisão lateral a frio. Essa incisão lateral facilita a introdução dos microenxertos por permitir a saída do ar e melhora sua fixação por conferir elasticidade ao orifício. Os pacientes foram previamente betabloqueados para evitar o efeito beta da adrenalina.

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Shilov, Georgii Nolianovich, and Vladislav Adamovich Ivanyutin. "Antioxidant activity of catecholamines as a chane of them antistress effect." Reviews on Clinical Pharmacology and Drug Therapy 12, no. 2 (2014): 43–46. http://dx.doi.org/10.17816/rcf12243-46.

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The antioxidant activity of some native catecholamines (adrenaline, noradrenaline, dopamine), water-soluble antioxidant emoxipine, agonist (apomorphine) and antagonist (haloperidol) of dopamine receptors was assessed as their influence on malonic dialdehyde content and products of lipid peroxidation in homogenates and suspension of the rat cortical brain cells. All catecholamines (adrenaline, noradrenaline, dopamine in concentrations of 10-4 M and 10-5 M) possessed a high (compartable with emoxipine) antioxidant activity. The most antioxidant effect was registered in apomorphine. The inhibitor

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JUšKA, Alfonsas, and Richard W. FARNDALE. "Inhibition of human platelet adenylate cyclase activity by adrenaline, thrombin and collagen: analysis and reinterpretation of experimental data." Biochemical Journal 340, no. 1 (1999): 245–53. http://dx.doi.org/10.1042/bj3400245.

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Mathematical models based on the current understanding of stimulation and inhibition of adenylate cyclase (AC) activity have been developed and used to analyse experimental data [Farndale, Winkler, Martin and Barnes (1992) Biochem. J. 282, 25-32] describing the inhibition of human platelet AC by collagen, thrombin and adrenaline. Here it has been demonstrated that neither affinities of receptors specific for adrenaline or thrombin nor the activity of cAMP phosphodiesterase are affected by collagen. Both collagen and thrombin at high doses act as effective inhibitors of AC activity. Inhibition

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29

el-Refai, M. F., and T. M. Chan. "Effects of adrenalectomy on binding to and actions of adrenergic receptors." Biochemical Journal 237, no. 2 (1986): 527–31. http://dx.doi.org/10.1042/bj2370527.

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Adrenalectomy results in significant changes in the mechanism of adrenergic activation of hepatic glycogenolysis. In adrenalectomized rats a greater role for the beta-adrenergic receptor is observed, whereas the alpha 1-adrenergic-mediated phosphorylase activation declines. Our present findings document that adrenalectomy causes a significant decrease in the high-affinity population of the alpha 1-adrenergic receptor labelled with [3H]adrenaline. Our data indicate a large increase in the number of beta-adrenergic binding sites after adrenalectomy. This increase was not consistent with the obse

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Jamieson, G. A., A. K. Agrawal, N. J. Greco, et al. "Phencyclidine binds to blood platelets with high affinity and specifically inhibits their activation by adrenaline." Biochemical Journal 285, no. 1 (1992): 35–39. http://dx.doi.org/10.1042/bj2850035.

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The ion channel probe phencyclidine [1-(1-phenylcyclohexyl)piperidine; PCP] selectively inhibited aggregation, secretion and ultrastructural changes in platelets induced by adrenaline, but did not affect activation induced by other common platelet agonists such as alpha-thrombin, ADP, collagen or ionophore A23187. [3H]PCP bound to platelets with high affinity (Kd 134 +/- 33 nM; 3600 +/- 1020 sites/platelet), as did the thienyl analogue [3H]TCP (1-[1-(2-thienyl)cyclohexyl]piperidine). PCP binding to platelets was increased 3-4-fold in N-methylglucamine buffer in the absence of Na+ ions. Binding

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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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32

Jones, C. R., R. McCabe, C. A. Hamilton, and J. L. Reid. "Maternal and Fetal Platelet Responses and Adrenoceptor Binding Characteristics." Thrombosis and Haemostasis 53, no. 01 (1985): 095–98. http://dx.doi.org/10.1055/s-0038-1661244.

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SummaryPaired blood samples were obtained from mothers (venous) and babies (cord venous blood) at the time of delivery by caesarean section under epidural anaesthetic. Fetal platelets failed to aggregate in response to adrenaline in vitro although adrenaline could potentiate the threshold response to adenosine diphosphate (1 μM). Fetal platelet responses to collagen and 8 Arg vasopressin did not differ significantly from maternal responses. Maternal and fetal platelets also showed similar inhibition of aggregation after activation of adenylate cyclase (PGE1 and parathormone), in contrast to th

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Huda, S., and N. Akhter. "Modulation of oxidative stress by enalapril and valsartan in adrenaline treated rats: a comparative study." Bangladesh Medical Research Council Bulletin 40, no. 1 (2014): 25–30. http://dx.doi.org/10.3329/bmrcb.v40i1.20333.

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Angiotensin (Ang II) II is known to promote oxidative stress in acute myocardial infarction (AMI). Inhibition of renin angiotensin system (RAS) or blockade of Ang II receptors may therefore be effective in reducing oxidative stress during AMI. The study evaluates and compares the protective effect of Angiotensin Converting Enzyme (ACE) inhibitor and AT1 receptor blocker in adrenaline induced oxidative stress in rats. Rats were treated with two successive injections of adrenaline subcutaneously at a dose of 2 mg/kg administered 24 hours apart. In other two groups of rats enalapril (30 mg/kg) or

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Güse-Behling, H., M. Ehrhart-Bornstein, S. R. Bornstein, M. R. Waterman, W. A. Scherbaum, and G. Adler. "Regulation of adrenal steroidogenesis by adrenaline expression of cytochrome P450 genes." Journal of Endocrinology 135, no. 2 (1992): 229–37. http://dx.doi.org/10.1677/joe.0.1350229.

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ABSTRACT The effect of adrenaline on the secretion of cortisol and cyclic AMP (cAMP) and on the accumulation of four different mRNAs encoding cholesterol side-chain cleavage cytochrome P450 (P450scc), 17α-hydroxylase cytochrome P450 (P45017α), 21-hydroxylase cytochrome P450 (P450c21) and 11β-hydroxylase cytochrome P450 (P45011β) was studied in bovine adrenocortical cells in primary culture and compared with the effects of ACTH. Treatment of cultured cells with adrenaline (1–100 μmol/l) showed a biphasic response in cortisol release over 1–24 h. Concentration of cAMP in the culture media increa

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Minuz, Pietro, Laura Fumagalli, Stefania Gaino, et al. "Rapid stimulation of tyrosine phosphorylation signals downstream of G-protein-coupled receptors for thromboxane A2 in human platelets." Biochemical Journal 400, no. 1 (2006): 127–34. http://dx.doi.org/10.1042/bj20061015.

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Signals ensuing from trimeric G-protein-coupled receptors synergize to induce platelet activation. At low doses, the thromboxane A2 analogue U46619 does not activate integrin αIIbβ3 or trigger platelet aggregation, but it induces shape changes. In the present study, we addressed whether low doses of U46619 trigger tyrosine phosphorylation independently of integrin αIIbβ3 activation and ADP secretion, and synergize with adrenaline (epinephrine) to induce aggregation in acetylsalicylic acid (aspirin)-treated platelets. Low doses of U46619 triggered tyrosine phosphorylation of different proteins,

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36

Vieira, Vânia L. Pimentel, Bernardo Baldisserotto, and Sílvia Krause. "Effect of acetylcholine, pilocarpine, serotonin and adrenaline on the in vitro gastric motility of Hoplias malabaricus (Teleostei)." Ciência e Natura 19, no. 19 (1997): 31. http://dx.doi.org/10.5902/2179460x26716.

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The in vitro effect of acetylcholine, pilocarpine, serotonina and adrenaline on gastric motility of the teleost Hoplias malabaricus was studied. The stomach of this specieshas spontaneous contractile activity, with no relationship between tension or frequency of contrations and fish weight. Acetylcholine reduced the frequency of contrations at higher concentrations, but had not effect at lower concentrations. The higher doses of this drug increased the tension and tonus of the contrations. Pilocarpine increased the frequency and tension of contractions at higher concentrations, but had not eff

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37

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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38

Newman-Tancredi, Adrian, Valérie Audinot-Bouchez, Alain Gobert, and Mark J. Millan. "Noradrenaline and adrenaline are high affinity agonists at dopamine D4 receptors." European Journal of Pharmacology 319, no. 2-3 (1997): 379–83. http://dx.doi.org/10.1016/s0014-2999(96)00985-5.

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39

Michel, Martin C. "Anger: Adrenaline receptors do not allow us to be too sinful." Biochemist 35, no. 6 (2013): 22–25. http://dx.doi.org/10.1042/bio03506022.

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All of us feel angry once in a while, but if anger turns into a chronic state of mind it is not only annoying to those around us, it may also make us ill. Much of the acute anger reaction is mediated by catecholamines acting on β-adrenoceptors. Chronic activation of these receptors leads to their desensitization, protecting us at least partly from the adverse effects of sustained anger.

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40

Schmidt, Karl T., and David Weinshenker. "Adrenaline Rush: The Role of Adrenergic Receptors in Stimulant-Induced Behaviors." Molecular Pharmacology 85, no. 4 (2014): 640–50. http://dx.doi.org/10.1124/mol.113.090118.

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Schrader, Thomas. "Towards Synthetic Adrenaline Receptors—Strong Binding of Amino Alcohols by Bisphosphonates." Angewandte Chemie International Edition in English 35, no. 22 (1996): 2649–51. http://dx.doi.org/10.1002/anie.199626491.

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42

Trumpp-Kallmeyer, Susanne, Jan Hoflack, Anne Bruinvels, and Marcel Hibert. "Modeling of G-protein-coupled receptors: application to dopamine, adrenaline, serotonin, acetylcholine, and mammalian opsin receptors." Journal of Medicinal Chemistry 35, no. 19 (1992): 3448–62. http://dx.doi.org/10.1021/jm00097a002.

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43

May, Clive N., Ian W. Ham, Kirsten E. Heslop, Frances A. Stone, and Christopher J. Mathias. "Intravenous morphine causes hypertension, hyperglycaemia and increases sympatho-adrenal outflow in conscious rabbits." Clinical Science 75, no. 1 (1988): 71–77. http://dx.doi.org/10.1042/cs0750071.

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1. In conscious rabbits, intravenous morphine (3 mg/kg) caused hypertension, bradycardia, hyperglycaemia and sedation. These changes were accompanied by large increases in plasma adrenaline and smaller increases in plasma noradrenaline. 2. These effects of morphine were prevented by intravenous naloxone, demonstrating their dependence on stimulation of opiate receptors. 3. Pretreatment with the antihistamines cimetidine and chlorpheniramine enhanced the morphine-induced rise in blood pressure, excluding a role for histamine release in the hypertensive action of morphine. 4. The centrally actin

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Sigola, L. B., and &. R. B. Zinyama. "Adrenaline inhibits macrophage nitric oxide production through beta1 and beta2 adrenergic receptors." Immunology 100, no. 3 (2000): 359–63. http://dx.doi.org/10.1046/j.1365-2567.2000.00029.x.

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Michelena, P., M. A. Moro, C. J. F. Castillo, and A. G. García. "Muscarinic receptors in separate populations of noradrenaline- and adrenaline-containing chromaffin cells." Biochemical and Biophysical Research Communications 177, no. 3 (1991): 913–19. http://dx.doi.org/10.1016/0006-291x(91)90625-h.

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46

Rapiejko, P. J., and C. C. Malbon. "Short-term hyperthyroidism modulates adenosine receptors and catalytic activity of adenylate cyclase in adipocytes." Biochemical Journal 241, no. 3 (1987): 765–71. http://dx.doi.org/10.1042/bj2410765.

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The effects of short-term hyperthyroidism in vivo on the status of the components of the fat-cell hormone-sensitive adenylate cyclase were investigated. The number of beta-adrenergic receptors was elevated by about 25% in membranes of fat-cells isolated from hyperthyroid rats as compared with euthyroid rats, but their affinity for radioligand was unchanged. Membranes of hyperthyroid-rat fat-cells displayed less than 65% of the normal complement of receptors for [3H]cyclohexyladenosine. The affinity of the receptors for this ligand was normal. In contrast with the marked increase in the amounts

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47

Grandt, R., K. Aktories, and K. H. Jakobs. "Evidence for two GTPases activated by thrombin in membranes of human platelets." Biochemical Journal 237, no. 3 (1986): 669–74. http://dx.doi.org/10.1042/bj2370669.

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Thrombin inhibits adenylate cyclase and stimulates GTP hydrolysis by high-affinity GTPase(s) in membranes of human platelets at almost identical concentrations. Both of these thrombin actions are similar to those observed with agonist-activated alpha 2-adrenoceptors coupling to the inhibitory guanine nucleotide-binding protein N1. However, stimulation of GTP hydrolysis caused by adrenaline (alpha 2-adrenoceptor agonist) and by thrombin at maximally effective concentrations was partially additive, whereas with regard to adenylate cyclase inhibition no additive response was observed. Furthermore

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48

Denis, C., H. Paris та J. C. Murat. "Hormonal control of fructose 2,6-bisphosphate concentration in the HT29 human colon adenocarcinoma cell line α2-adrenergic agonists counteract effect of vasoactive intestinal peptide". Biochemical Journal 239, № 3 (1986): 531–36. http://dx.doi.org/10.1042/bj2390531.

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Vasoactive intestinal peptide (VIP) was found to cause a dose-dependent decrease in fructose 2,6-bisphosphatase concomitant with an increase in cyclic AMP in cultured HT29 cancer cells from human colon. The maximum effect was a 41% decrease obtained with 10 nM-VIP, and half-maximum effect was obtained with 0.75 nM-VIP. The effect of 2.5 nM-VIP was almost totally counteracted (i.e. fructose 2,6-bisphosphate concentration was restored) by either adrenaline (1 microM) or the alpha 2-adrenergic agonist UK-14304 (1 microM); the alpha 2-agonist clonidine (1 microM) was less efficient, since the VIP

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Alhadeff, Raphael, Igor Vorobyov, Han Wool Yoon, and Arieh Warshel. "Exploring the free-energy landscape of GPCR activation." Proceedings of the National Academy of Sciences 115, no. 41 (2018): 10327–32. http://dx.doi.org/10.1073/pnas.1810316115.

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G-protein–coupled receptors (GPCRs) are a large group of membrane-bound receptor proteins that are involved in a plethora of diverse processes (e.g., vision, hormone response). In mammals, and particularly in humans, GPCRs are involved in many signal transduction pathways and, as such, are heavily studied for their immense pharmaceutical potential. Indeed, a large fraction of drugs target various GPCRs, and drug-development is often aimed at GPCRs. Therefore, understanding the activation of GPCRs is a challenge of major importance both from fundamental and practical considerations. And yet, de

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Hoffman, Brian B., та Gozoh Tsujimoto. "Direct measurement of vascular α1-adrenoceptors". Clinical Science 68, s10 (1985): 35s—37s. http://dx.doi.org/10.1042/cs068s035.

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1. α-Adrenoceptors play an important role in regulating vascular tone. [125I]BE2254, a high affinity antagonist, has been utilized to label α1-receptors in membrane preparations from rabbit aorta. [125I]BE2254 specifically labels a single class of binding sites with the characteristics of α1-receptors. 2. Catecholamines compete for [125I]BE2254 binding stereospecifically and with the characteristic α-adrenergic potency series (−)-adrenaline ≥ (−)-noradrenaline ≪ (−)-isoprenaline. 3. The α1-adrenoceptor selective antagonist prazosin is much more potent than yohimbine in competing for the [125I]

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