Relevant bibliographies by topics / Adrenalina - Receptores

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Adrenalina - Receptores'

Author: Grafiati
Published: 4 June 2021
Last updated: 1 February 2022

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Journal articles on the topic "Adrenalina - Receptores"

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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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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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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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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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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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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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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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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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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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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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Dissertations / Theses on the topic "Adrenalina - Receptores"

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Carvalho, Olga Maria Fernandes de 1953. "Transmissão do sinal insulinico em tecido adiposo : efeitos do jejum prolongado, do envelhecimento, da adrenalina e da dexametasona." [s.n.], 1997. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311217.

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Orientador: Mario Jose Abdalla Saad<br>Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas<br>Made available in DSpace on 2018-07-23T02:50:36Z (GMT). No. of bitstreams: 1 Carvalho_OlgaMariaFernandesde_D.pdf: 5088489 bytes, checksum: c39b531b63bc9ea9453d24625b77b369 (MD5) Previous issue date: 1997<br>Resumo: A insulina, ao se ligar à subunidade a. de seu receptor heterotetramérico, dá inicio à uma série de ações imediatas e tardias, metabólicas e promotoras de crescimento. Tais eventos ocorrem através da estimulação da subunidade J3 transmembrana do receptor, q
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Flores, Rafael Appel. "A expressão da proteína Fos após injeção intracerebroventricular de adrenalina em ratos saciados." reponame:Repositório Institucional da UFSC, 2014. https://repositorio.ufsc.br/xmlui/handle/123456789/129365.

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Dissertação (Mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências Biológicas, Programa de Pós-Graduação em Neurociências, Florianópolis, 2014<br>Made available in DSpace on 2015-02-05T21:00:20Z (GMT). No. of bitstreams: 1 329729.pdf: 1294677 bytes, checksum: ba08177546cfad8c54fd1c59d7f7a5a5 (MD5) Previous issue date: 2014<br>Estudos prévios em nosso laboratório sugerem que a injeção de adrenalina (AD) no núcleo mediano da rafe (NMR) diminui a ingestão de alimentos em ratos em restrição alimentar e aumenta a ingestão em ratos saciados. A injeção de agonista a-2 adrenérgico n
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Portes, Marina Aparecida Magnini. "Adrenalina e noradrenalina promovem a generalização da resposta de medo por ativarem receptores Alfa-1 e Beta adrenérgicos do córtex pré-límbico durante a consolidação de uma memória aversiva." Florianópolis, 2016. https://repositorio.ufsc.br/xmlui/handle/123456789/177526.

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Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Ciências Biológicas. Programa de Pós-Graduação em Farmacologia, Florianópolis, 2016<br>Submitted by Gesmar Kingeski Barbosa null (gesmar.k@ufsc.br) on 2017-07-14T12:12:29Z No. of bitstreams: 1 PFMC0332-D.pdf: 1550730 bytes, checksum: e0363dcfa48279c35ed5fb524419ef2e (MD5)<br>Made available in DSpace on 2017-07-14T12:12:29Z (GMT). No. of bitstreams: 1 PFMC0332-D.pdf: 1550730 bytes, checksum: e0363dcfa48279c35ed5fb524419ef2e (MD5) Previous issue date: 2016<br>Aprender e lembrar são processos essenciais para a sobrev
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Vanderlei, Luiz Carlos Marques. "Influencia do ciclo estral e do estresse sobre a sensibilidade as catecolamidas em atrios de ratas." [s.n.], 1996. http://repositorio.unicamp.br/jspui/handle/REPOSIP/288577.

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Orientadores: Regina Celia Spadari-Bratfisch, Maria Cecilia Ferraz de Arruda Veiga<br>Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Odontologia de Piracicaba<br>Made available in DSpace on 2018-07-21T21:21:08Z (GMT). No. of bitstreams: 1 Vanderlei_LuizCarlosMarques_D.pdf: 4027500 bytes, checksum: a03c4378fdc093ef837a0eb1f83250ac (MD5) Previous issue date: 1996<br>Resumo: O objetivo desse trabalho foi analisar as alterações de sensibilidade às catecolaminas em átrios direitos isolados (AD) de ratas submetidas a estresse por choques nas patas e sacrificadas no estro ou die
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Marcondes, Fernanda Klein 1970. "Influencia do sexo e das fases do ciclo estral sobre a reação de estresse em ratos." [s.n.], 1995. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314630.

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Orientador: Regina Celia Spadari-Bratfisch<br>Dissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia<br>Made available in DSpace on 2018-07-20T12:32:13Z (GMT). No. of bitstreams: 1 Marcondes_FernandaKlein_M.pdf: 4667978 bytes, checksum: f9546f7c08e60c1479f7c335ad4626f3 (MD5) Previous issue date: 1995<br>Resumo: Estudamos a influência do sexo e das fases do ciclo estral sobre a reação de estresse em ratos submetidos à natação, a 30°C. Analisamos as alterações de sensibilidade às catecolaminas em átrios direitos isolados e as concentrações plasmáticas de corticostero
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Fleury, Camila de Assis. "Avaliação dos efeitos vasculares e expressão de mRNA de receptores de drogas vasoconstritoras em leito arterial mesentérico de ratos normotensos, diabéticos, hipertensos renais um-rim, um clip (1R-1C) e 1R-1C diabéticos." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/25/25149/tde-03052017-192648/.

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O presente trabalho teve como objetivo avaliar e comparar a reatividade vascular de agentes vasoconstritores presentes nas soluções anestésicas locais (Adrenalina - vasoconstrição e vasodilatação; Felipressina - vasoconstrição), nas doses de 80, 160, 320, 640 e 1280ng (adrenalina) ou 0,25; 0,5; 1; 2 e 4 x10-3UI (felipressina), em leito arterial mesentérico deratos normotensos, diabéticos, hipertensos renais um-rim, um-clip (1R-1C) e hipertensos1R-1C-diabéticos. E correlacionar tal reatividadecom expressão de RNAm dos receptores 1A e 2- adrenérgicos, V1A para vasopressina e AT1A, AT1Be AT2 para
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Galindo, Tovar Alejandro. "Control por fosfodiesterasas de la función cardíaca activada por los receptores acoplados a la proteína Gs." Doctoral thesis, Universidad de Murcia, 2009. http://hdl.handle.net/10803/10798.

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Los receptores &#946;-adrenérgicos (&#946;AR) y de serotonina (5-HT4) median sus efectos en tejidos cardiacos a través de la ruta receptor-Gs-AC-AMPc. Las fosfodiesterasas (PDE) son una amplia familia de enzimas cuya función es la degradación del AMPc. Se desconocía que isoenzimas de PDEs son responsables de la hidrólisis de AMPc en las diferentes regiones cardiacas. El objetivo de esta tesis doctoral es investigar que isoenzimas de PDEs tienen actividad en el miocardio humano, porcino y de roedores. Se han realizado estudios cronotrópicos, inotrópicos, lusitrópicos, bioquímicos y electrofisio
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Costa, Alexandre Jayme Lopes Dantas. "Efeitos do treinamento físico sobre a função cardíaca e as propriedades mecânicas em cardiomiócitos de camundongos knockout para os receptores β2-adrenérgicos". Universidade Federal de Viçosa, 2018. http://www.locus.ufv.br/handle/123456789/22192.

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Submitted by MARCOS LEANDRO TEIXEIRA DE OLIVEIRA (marcosteixeira@ufv.br) on 2018-10-08T12:38:35Z No. of bitstreams: 1 texto completo.pdf: 1787653 bytes, checksum: d47fa7116143fe4f93ee855509e5e86a (MD5)<br>Made available in DSpace on 2018-10-08T12:38:35Z (GMT). No. of bitstreams: 1 texto completo.pdf: 1787653 bytes, checksum: d47fa7116143fe4f93ee855509e5e86a (MD5) Previous issue date: 2018-08-27<br>O objetivo do presente estudo foi investigar os efeitos do exercício aeróbico continuo de intensidade moderada (EACM) sobre as propriedades mecanicas e funcionais de cardiomiócitos de camundong
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Ribeiro, Carlos Alberto da Silva [UNESP]. "Investigação do envolvimento de subtipos de adrenoceptores α1 no efeito anti-imobilidade da imipramina no teste de suspensão pela cauda". Universidade Estadual Paulista (UNESP), 2015. http://hdl.handle.net/11449/123303.

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Made available in DSpace on 2015-05-14T16:53:19Z (GMT). No. of bitstreams: 0 Previous issue date: 2015-02-27Bitstream added on 2015-05-14T16:59:01Z : No. of bitstreams: 1 000828052_20150610.pdf: 305956 bytes, checksum: 7369e2c8e287bd85ed19449e6cb2b2e6 (MD5) Bitstreams deleted on 2015-06-12T11:19:08Z: 000828052_20150610.pdf,. Added 1 bitstream(s) on 2015-06-12T11:19:39Z : No. of bitstreams: 1 000828052.pdf: 458163 bytes, checksum: 8f3277eff5562c7da6c209cf3706a1c0 (MD5)<br>A imipramina é antidepressivo tricíclico cujo principal mecanismo é a inibição da captura neuronal de noradrenalina e/ou
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Ribeiro, Carlos Alberto da Silva. "Investigação do envolvimento de subtipos de adrenoceptores α1 no efeito anti-imobilidade da imipramina no teste de suspensão pela cauda /". Botucatu, 2015. http://hdl.handle.net/11449/123303.

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Orientador: André Sampaio Pupo<br>Banca: Ana Lúcia Severo Rodrigues<br>Banca: Ricardo Luiz Nunes de Souza<br>Banca: Márcia Gallacci<br>Banca: Leonardo Resstel Barbosa Moraes<br>Resumo: A imipramina é antidepressivo tricíclico cujo principal mecanismo é a inibição da captura neuronal de noradrenalina e/ou serotonina, aumentando os níveis sinápticos dessas monoaminas. Além disso, a imipramina, bem como outros antidepressivos tricíclicos, antagonizam os adrenoceptores α1 na mesma faixa de concentração em que inibem o transportador de noradrenalina. Por outro lado, estudos recentes mostraram que a
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Books on the topic "Adrenalina - Receptores"

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Advances in adrenergic receptor biology. Elsevier, 2011.

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Fiziologicheskai͡a rolʹ autoadrenoret͡septorov. "Nauka", 1991.

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Congreso de Drogodependencias (1987 San Sebastián, Spain). Conference on drug addiction: San Sebastian, Basque country, 7th-11th September, 1987 = Drogazaletasun Biltzarra : Donostia, Euskal Herria, 1987 Ko Irailak 7-11. Edited by García Sevilla Jesús A and Congreso Mundial Vasco. (2nd : 1987 : San Sebastián, Spain, etc.). J.R. Prous, 1988.

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Perez, Dianne M. The Adrenergic Receptors in the 21st Century (The Receptors). Humana Press, 2005.

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1945-, Insel Paul A., ed. Adrenergic receptors in man. Dekker, 1987.

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1943-, Lefkowitz Robert J., and Lindenlaub E, eds. Adrenergic receptors: Molecular properties and therapeutic implications. Schattauer Varlag, 1985.

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M, Perez Dianne, ed. The adrenergic receptors: In the 21st century. Humana Press, 2005.

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R, Ruffolo Robert, ed. Adrenoceptors: Structure, function and pharmacology. Harwood Academic Publishers, 1995.

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E, Szabadi, Bradshaw C. M, and International Congress of Pharmacology (11th : 1990 : Amsterdam, Netherlands), eds. Adrenoceptors: Structure, mechanisms, function. Birkhäuser Verlag, 1991.

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E, Szabadi, Bradshaw C. M, Nahorski S. R, International Union of Pharmacology, and International Congress of Pharmacology (9th : 1984 : London, England), eds. Pharmacology of adrenoceptors. VCH, 1985.

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Book chapters on the topic "Adrenalina - Receptores"

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Gorain, Bapi, Sulagna Dutta, Utpal Nandy, Pallav Sengupta, and Hira Choudhury. "Pharmacology of Adrenaline, Noradrenaline, and Their Receptors." In Frontiers in Pharmacology of Neurotransmitters. Springer Singapore, 2020. http://dx.doi.org/10.1007/978-981-15-3556-7_4.

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Gilsbach, Ralf, and Lutz Hein. "Presynaptic Metabotropic Receptors for Acetylcholine and Adrenaline/Noradrenaline." In Handbook of Experimental Pharmacology. Springer Berlin Heidelberg, 2008. http://dx.doi.org/10.1007/978-3-540-74805-2_9.

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Prüll, Cay-Rüdiger, Andreas-Holger Maehle, and Robert Francis Halliwell. "The Dual Adrenalin Receptor Theory of Raymond P. Ahlquist (1914–83) and its Application in Drug Development between 1950 and 1970." In A Short History of the Drug Receptor Concept. Palgrave Macmillan UK, 2009. http://dx.doi.org/10.1057/9780230583740_7.

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"8. Lock and Key: Receptors for Adrenaline." In Adrenaline. Harvard University Press, 2013. http://dx.doi.org/10.4159/harvard.9780674074712.c9.

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"Urticarial rashes." In Paediatric Dermatology, edited by Sue Lewis-Jones and Ruth Murphy. Oxford University Press, 2020. http://dx.doi.org/10.1093/med/9780198821304.003.0021.

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This chapter covers definitions of urticaria, angioedema (acute and chronic), and dermographism. Urticaria pathogenesis and causes/trigger factors are discussed (idiopathic, drugs, contact, allergic, physical, and possible associated systemic diseases). Assessment is highlighted and guidance given on investigations. The urticaria management section covers general recommendations, first-line therapy (including antihistamines, and where appropriate for severe cases systemic steroids and adrenaline) and second-line treatments (leukotriene receptor antagonists, anti-IgE therapy, and systemic immunosuppressive agents). Angioedema subtypes (ordinary, hereditary, and acquired) are discussed, relevant investigations, and also management of both acute angioedema and therapies used for prophylaxis. The anaphylaxis section covers the definition, symptoms, and management, including adrenaline actions, age-related doses and current injectable devices, antihistamine, and steroid age-appropriate doses, and general supportive measures. A separate section covers the differential diagnoses of urticarial rashes, including neonatal and infantile rashes, moving annular urticated rashes, fixed annular urticated rashes, urticarial rash with angioedema, and urticarial rashes with systemic symptoms, helping the reader to narrow down the possible differential diagnoses when confronted with a patient with an urticarial rash.
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Kieschke, J., S. Mense, and N. R. Prabhakar. "Chapter 12 Influence of adrenaline and hypoxia on rat muscle receptors in vitro." In Progress in Brain Research. Elsevier, 1988. http://dx.doi.org/10.1016/s0079-6123(08)63003-4.

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Wallace, Daniel J., and Janice Brock Wallace. "What is the Autonomic Nervous System?" In All About Fibromyalgia. Oxford University Press, 2002. http://dx.doi.org/10.1093/oso/9780195147537.003.0013.

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The autonomic nervous system (ANS) has already been introduced; let’s summarize what we know about it so far. Part of the peripheral nervous system, the ANS consists of the sympathetic nervous system (SNS), which consists of outflow from the thoracic and upper lumbar spine, and the parasympathetic nervous system (PNS), including outflow from the cranial nerves emanating from the upper spine and also from the mid-lumbar to the sacral areas at the buttock region. Several neurochemicals help transmit autonomic instructions. These include epinephrine (adrenaline), norepinephrine (noradrenalin), dopamine, and acetylcholine. This chapter will focus on how abnormalities in the regulation of the ANS cause many of the symptoms and signs observed in fibromyalgia. Our body has numerous receptors or surveillance sensors that detect heat, cold, and inflammation. These ANS sensors perform a function known as autoregulation. As an example of how the ANS normally works, why don’t we pass out when we suddenly jump out of bed? Because the ANS instantly constricts our blood vessels peripherally and dilates them centrally. In other words, as blood is pooled to the heart and the brain, the ANS adjusts our blood pressure and regulates our pulse, or heart rate, so that we don’t collapse. On the local level, these sensors dilate or constrict flow from blood vessels. They can secondarily contract and relax muscles, open and close lung airways, or cause us to sweat. For instance, ANS sensors can tone muscles, regulate urine, and regulate bowel movements, as well as dilate or constrict our pupils. The SNS arm of the ANS is our “fight or flight” system, releasing epinephrine and norepinephrine as well as a neurochemical called dopamine. Whereas the SNS often acts as an acute stress response, the PNS arm tends to protect and conserve body processes and resources. The SNS and PNS sometimes work at cross purposes, but frequently they work together to permit actions such as normal sexual functioning and urination. How do the workings of the ANS relate to fibromyalgia? The SNS is underactive in fibromyalgia in the sense that an increased ratio of excitatory to inhibitory responses from central sensitization results in lower blood flow rates, leaky capillaries, at relatively low baseline blood pressure.
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Fuxe, K., L. F. Agnati, A. Härfstrand, et al. "Chapter 20 Morphofunctional studies on the neuropeptide Y/adrenaline costoring terminal systems in the dorsal cardiovascular region of the medulla oblongata. Focus on receptor-receptor interactions in cotransmission." In Progress in Brain Research. Elsevier, 1986. http://dx.doi.org/10.1016/s0079-6123(08)60246-0.

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Conference papers on the topic "Adrenalina - Receptores"

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Grant, P. J., P. G. Wiles, M. Boothby, J. A. Davies, and C. R. M. Prentice. "EFFECTS OF VASOPRESSIN AND ADRENALINE ON FIBRINOLYSIS: SYNERGISTIC OR ADDITIVE?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644136.

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Vasopressin (aVP) andadrenalineboth enhance plasminogenactivator activity when infused at low doses in man and probably act asphysiological regulators of fibrinolysis under certain conditions. Therelative contributions of these hormones to changes in fibrinolysis are unknown. This study was carried out to investigate whether aVP and adrenaline act synergistically on plasminogen activator in man. Four normal volunteers were infused with (1) aVP (1. OU/h), (2) adrenaline (420 μg/h), (3) aVP and adrenaline and(4) 0.9% saline for 1h. Saline (0.9%) wasinfused for 30 min before and afterinfusion. Th
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Watts, I. S., R. J. Keery, and P. Lumley. "DIFFERENTIAL EFFECT OF TEMPORARY Ca2+ DEPRIVATION UPON ADP-AND COLLAGEN-INDUCED PLATELET AGGREGATION IN HUMAN WHOLE BLOOD." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644467.

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In platelets exposed to chelating agents at 37°C and recalcified, aggregation to ADP, adrenaline, collagen and thrombin were either abolished or markedly reduced (1). This phenomenon has been suggested to be caused by disruption, by Ca2+ deprivation, of the fibrinogen receptor (glycoprotein lib Ilia complex) on the surface of the platelet (2). This effect was dependent on the exposure time of Ca2+ chelators and was reduced at lower temperatures. We have investigated the effect of exposure of human platelets to EGTA upon aggregation to a range of agonists at both 37 and 25°C. EGTA (5 mM) was in
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Lande, K., I. O. S. S. E. Kieldsen, A. Westheim, et al. "PATIENTS WITH MILD ESSENTIAL HYPERTENSION HAVE INCREASED PLATELET SIZE AND RELEASE REACTION ANO SHOW INCREASED RECEPTOR RESPONSE TO INFUSED ADRENALINE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644261.

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Hypertensive (n = 35) and normotensive {n = 44) men all 42 years old were studied. The hypertensive (HT) had larger venous platelets than the normotensive (HT) (7.46 ± 0.10 vs 7.12 ± 0.09 10-15 1, p = 0.01). Plasma concentration of |3-thromboglobulin (BTG) was increased in arterial blood in hypertensive (40 ± 8 vs 21 ± 2 ug/1, p=0.02) while the venous values were similar in the two groups. Despite similar sampling procedure, the normotensive subjects had markedly higher BTGconcentration in venous compared to arterial blood (p≺0.01) at variance from thehypertensive where the arteriovenous diffe
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Hopple, Sara, Mark Bushfield, Fiona Murdoch, and D. Euan MacIntyre. "REGULATION OF PLATELET cAMP FORMATION BY PROTEIN KINASE C." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644512.

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Exogenous synthetic 1,2-diacylglycerols (e.g. 1,2-dioctanoylglycerol, DiC8) and 4β Phorbol esters (e.g. phorbol myristate acetate, PMA) routinely are used to probe the effects of protein Kinase C (PKC) on cellular responsiveness. Such agents act either independently or synergistically with elevated [Ca2+]i to induce platelet activation, but also inhibit agonist-induced inositol lipid metabolism and Ca2+ flux. These findings led to the concept that activated PKC can function as a bi-directional regulator of platelet reactivity. Therefore, DiCg and PMA were utilized to examine the effects of act
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Gladwin, A. M., and J. Martin. "ARACHIDONIC ACID (AA) INDUCED AGGREGATION OF RAT PRO- MEGAKARYOBLASTS (RPM)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643542.

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Platelet aggregation can be induced in vitro by a variety of platelet agonists acting upon membrane receptors. Since platelets have only a limited ability to synthesise proteins, these receptors must be present in megakaryocytes. This was investigated using an eternal line line of RPMs. Cells were suspended in rat platelet free plasma (PFP) at a concentration of 105 cells ml-1 . 200μl aliquots of this were placed in a light aggregometer. For this suspension, and for an aliquot of PFP, light transmission was adjusted to zero and 100% respectively. Addition of ADP (plasma concentrations 1-100μM)
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Hattori, A., R. Nagayama, I. Fuse, T. Takeshige, S. Takizawa, and A. Shibata. "FURTHER CHARACTERIZATION OF PLATELET RELEASE MECHANISM DEFECT WITH DEFECTIVE A23187 AGGREGATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644878.

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In order to clarify the basic abnormality of patients with release mechanism abnormality with defective response to A23187 (A23) (Hattori et al. Acta Haematol. Jap. 44:969, 1981), the proband (female) showing a life long mild hemorrhagic tendency was further examined. Her platelet (pit) count, morphology, storage pool was normal. Bleeding time (Duke) was more than 15 min.PRP-aggregation (Ag) was normal when induced by PMA, whereas decreased (only primary Ag) by ADP, adrenalin, arachidonate (AA) (−2mM), Tx analog STA2 (−4μM), PAF (−10μM). Ag was defective in response to A23 (−40μM), Ag using wa
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Bevan, Jane, and S. Heptinstall. "BOW CAN WE INHIBIT 5HT-INDUCED PLATELET AGGREGATION AND WHY SHOULD WE BOTHER?" In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643853.

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Platelets are induced to aggregate when 5-hydraxytryptamine (5HT) is added to citrated whole blood and the extent of aggregation can be measured using a Whole Blood Platelet Counter. We have used this method to study a) 5HT-induced platelet aggregation in normal human blood and the effects of 14 5HT receptor antagonists and 2 Ca++-channel blockers, and b) aggregation in blood from patients with peripheral vascular disease (PVD). Previous studies of platelet aggregation in platelet-rich plasma have indicated an increased platelet sensitivity to 5HT in PVD, and a multicentre study of ketanserin
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Lanza, M., A. Beretz, A. Stierlé, D. Hanau, M. Kubina, and J. P. Cazenave. "ADRENALINE ACTIVATES HUMAN PLATELETS BUT IS NOT PER SE AN AGGREGATING AGENT. EFFECTS ON PLATELET MORPHOLOGY, MEMBRANEFLUIDITY, FIBRINOGEN BINDING, CYTOPLASMIC FREE CALCIUM AND PROTEIN PHOSPHORYLATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643762.

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Adrenaline (Adr) is generally considered as a full agonist able to induce in vitro the aggregation of human platelets and could play an important role in vivo in the appearance of thrombotic disorders when catecholamine levels are increased. Adr 2.5 M) induces the aggregation and secretion of 41 % of preloaded 3H-serotonin in human platelets in citrated plasma. This effect is not seen in plasma collected on 50 ATU/ml hirudin, and is due to the generation of traces of thrombin during blood collection and not to a direct effect of citrate itself, such asthe lowering of plasma free calcium. With
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Lumley, P., E. W. Collington, P. Hallett, et al. "THE EFFECTS OF GR32191, A NEW THROMBOXANE RECEPTOR BLOCKING DRUG,ON PLATELETS AND VASCULAR SMOOTH MUSCLE IN VITRO." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643754.

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The effect of a new thromboxane receptor blocking drug GR32191 ([1R-[1α(Z),2β,3β,5α]]-(+)-7-[5-[[(1,1"-biphenyl)-4-yl]methoxy] -3-hydroxy-2-(l-piperidinyl)cyclopentyl]-4-heptenoic acid,hydrochloride) has been examined upon platelets and vascular smooth muscle. In human platelet-rich plasma (PRP), aggregation to thromboxane(Tx) A2, PGH2, arachidonic acid, collagen andU-46619 was antagonised by GR32191 (IC50 range 2-36 nM).Primary aggregation (PRP treated with aspirin 10 pM) to ADP, 5-HT and adrenaline were unaffected by concentrations of GR32191 up to 10 pM. In human PRP, U-46619-induced aggreg
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De Clerck, F., R. Van de Wiele, B. Xhonneux, et al. "PLATELET TXA2 SYNTHETASE INHIBITION AND TXA2/PROSTAGLANDIN ENDOPEROXIDE RECEPTOR BLOCKADE COMBINED IN ONE MOLECULE (R 68070)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643465.

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F 68070, an oxime-alkane carboxylic acid derivative (Janssen Pharmaceutica), is a potent inhibitor of thromboxane A2 (TXA2) synthetase activity (IC50 in vitro against thrombin-stimulated human platelets in plasma : R 68070 : 2.9 x 10-8 M; CGS 13080 : 6 x 10-8 M; OKY-1581 : 8.2 x 10-8 M; dazmegrel : 2.6 x 10-8 M; dazoxiben : 2.3 x 10-8 M).The compound specifically inhibits platelet TXA2 synthetase activity (14C-arachidonic acid metabolism by washed human platelets) without effect on the cyclo-oxygenase, lipoxygenase (platelets, RBL cells) or prostacyclin synthetase activities (rat aortic rings)
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