Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels

Detalhes bibliográficos
Autor(a) principal: Fauaz, Grasiele
Data de Publicação: 2000
Outros Autores: Feres, Teresa, Borges, Antonio CR [UNIFESP], Paiva, Therezinha B. [UNIFESP]
Tipo de documento: Artigo
Idioma: eng
Título da fonte: Repositório Institucional da UNIFESP
Texto Completo: http://repositorio.unifesp.br/handle/11600/26388
http://dx.doi.org/10.1038/sj.bjp.0703630
Resumo: 1 the role of alpha (2)-adrenoceptors in the response of aorta smooth muscle rings to the alpha (2)- adrenoceptors agonists UK 14,304 and clonidine was studied.2 Stimulation by 1-10 nM UK 14,304 caused dose-dependent relaxant responses in BaCl2-contracted endothelium-denuded aorta rings, and hyperpolarization in rings with or without endothelium. which were inhibited by yohimbine and glibenclamide, but not affected by prazosin, propranolol, apamin or iberiotoxin. At higher concentrations (10 nM- 10 muM) UK 14,304 also induced a depolarizing effect which was potentiated by yohimbine and inhibited by prazosin. These results indicate that UK 14,304 acts on alpha (2)-adrenoceptors at lower concentrations and on both alpha (1)- and alpha (2)-adrenoceptors above 10 nM.3 in rings, with or without endothelium, noradrenaline had a depolarizing effect which was inhibited by prazosin. Adrenaline did not affect the membrane potential but in the presence of prazosin caused hyperpolarization, which was inhibited by yohimbine and glibenclamide. These results indicate that noradrenaline is more selective for alpha (1)-, whereas adrenaline has similar affinities for alpha (1)- acid alpha (2)-adrenoceptors.4 in aortae with endothelium, L-NNA caused a small depolarization but did not affect the hyperpolarization induced by UK 14,304, indicating that NO is not involved in that response.5 Glibenclamide induced a small depolarization in aortae, with or without endothelium, indicating that ATP-sensitive K+ channels may play a role in maintaining the smooth muscle's membrane potential.6 Our results indicate that, in rat aorta, alpha (2)-adrenoceptors are also present in the smooth muscle, and that these receptors act through small-conductance ATP-sensitive K+ channels.
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spelling Fauaz, GrasieleFeres, TeresaBorges, Antonio CR [UNIFESP]Paiva, Therezinha B. [UNIFESP]Universidade Federal de São Paulo (UNIFESP)2016-01-24T12:31:11Z2016-01-24T12:31:11Z2000-10-01British Journal of Pharmacology. Basingstoke: Nature Publishing Group, v. 131, n. 4, p. 788-794, 2000.0007-1188http://repositorio.unifesp.br/handle/11600/26388http://dx.doi.org/10.1038/sj.bjp.070363010.1038/sj.bjp.0703630WOS:0000900371000201 the role of alpha (2)-adrenoceptors in the response of aorta smooth muscle rings to the alpha (2)- adrenoceptors agonists UK 14,304 and clonidine was studied.2 Stimulation by 1-10 nM UK 14,304 caused dose-dependent relaxant responses in BaCl2-contracted endothelium-denuded aorta rings, and hyperpolarization in rings with or without endothelium. which were inhibited by yohimbine and glibenclamide, but not affected by prazosin, propranolol, apamin or iberiotoxin. At higher concentrations (10 nM- 10 muM) UK 14,304 also induced a depolarizing effect which was potentiated by yohimbine and inhibited by prazosin. These results indicate that UK 14,304 acts on alpha (2)-adrenoceptors at lower concentrations and on both alpha (1)- and alpha (2)-adrenoceptors above 10 nM.3 in rings, with or without endothelium, noradrenaline had a depolarizing effect which was inhibited by prazosin. Adrenaline did not affect the membrane potential but in the presence of prazosin caused hyperpolarization, which was inhibited by yohimbine and glibenclamide. These results indicate that noradrenaline is more selective for alpha (1)-, whereas adrenaline has similar affinities for alpha (1)- acid alpha (2)-adrenoceptors.4 in aortae with endothelium, L-NNA caused a small depolarization but did not affect the hyperpolarization induced by UK 14,304, indicating that NO is not involved in that response.5 Glibenclamide induced a small depolarization in aortae, with or without endothelium, indicating that ATP-sensitive K+ channels may play a role in maintaining the smooth muscle's membrane potential.6 Our results indicate that, in rat aorta, alpha (2)-adrenoceptors are also present in the smooth muscle, and that these receptors act through small-conductance ATP-sensitive K+ channels.Universidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Biophys, BR-04023062 São Paulo, BrazilWeb of Science788-794engNature Publishing GroupBritish Journal of Pharmacologyrat aortamembrane potentialalpha-2 adrenoceptorATP-sensitive K+ channelUK 14,304Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channelsinfo:eu-repo/semantics/publishedVersioninfo:eu-repo/semantics/articleinfo:eu-repo/semantics/openAccessreponame:Repositório Institucional da UNIFESPinstname:Universidade Federal de São Paulo (UNIFESP)instacron:UNIFESP11600/263882022-09-27 11:31:12.74metadata only accessoai:repositorio.unifesp.br:11600/26388Repositório InstitucionalPUBhttp://www.repositorio.unifesp.br/oai/requestopendoar:34652022-09-27T14:31:12Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)false
dc.title.en.fl_str_mv Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels
title Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels
spellingShingle Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels
Fauaz, Grasiele
rat aorta
membrane potential
alpha-2 adrenoceptor
ATP-sensitive K+ channel
UK 14,304
title_short Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels
title_full Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels
title_fullStr Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels
title_full_unstemmed Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels
title_sort Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels
author Fauaz, Grasiele
author_facet Fauaz, Grasiele
Feres, Teresa
Borges, Antonio CR [UNIFESP]
Paiva, Therezinha B. [UNIFESP]
author_role author
author2 Feres, Teresa
Borges, Antonio CR [UNIFESP]
Paiva, Therezinha B. [UNIFESP]
author2_role author
author
author
dc.contributor.institution.none.fl_str_mv Universidade Federal de São Paulo (UNIFESP)
dc.contributor.author.fl_str_mv Fauaz, Grasiele
Feres, Teresa
Borges, Antonio CR [UNIFESP]
Paiva, Therezinha B. [UNIFESP]
dc.subject.eng.fl_str_mv rat aorta
membrane potential
alpha-2 adrenoceptor
ATP-sensitive K+ channel
UK 14,304
topic rat aorta
membrane potential
alpha-2 adrenoceptor
ATP-sensitive K+ channel
UK 14,304
description 1 the role of alpha (2)-adrenoceptors in the response of aorta smooth muscle rings to the alpha (2)- adrenoceptors agonists UK 14,304 and clonidine was studied.2 Stimulation by 1-10 nM UK 14,304 caused dose-dependent relaxant responses in BaCl2-contracted endothelium-denuded aorta rings, and hyperpolarization in rings with or without endothelium. which were inhibited by yohimbine and glibenclamide, but not affected by prazosin, propranolol, apamin or iberiotoxin. At higher concentrations (10 nM- 10 muM) UK 14,304 also induced a depolarizing effect which was potentiated by yohimbine and inhibited by prazosin. These results indicate that UK 14,304 acts on alpha (2)-adrenoceptors at lower concentrations and on both alpha (1)- and alpha (2)-adrenoceptors above 10 nM.3 in rings, with or without endothelium, noradrenaline had a depolarizing effect which was inhibited by prazosin. Adrenaline did not affect the membrane potential but in the presence of prazosin caused hyperpolarization, which was inhibited by yohimbine and glibenclamide. These results indicate that noradrenaline is more selective for alpha (1)-, whereas adrenaline has similar affinities for alpha (1)- acid alpha (2)-adrenoceptors.4 in aortae with endothelium, L-NNA caused a small depolarization but did not affect the hyperpolarization induced by UK 14,304, indicating that NO is not involved in that response.5 Glibenclamide induced a small depolarization in aortae, with or without endothelium, indicating that ATP-sensitive K+ channels may play a role in maintaining the smooth muscle's membrane potential.6 Our results indicate that, in rat aorta, alpha (2)-adrenoceptors are also present in the smooth muscle, and that these receptors act through small-conductance ATP-sensitive K+ channels.
publishDate 2000
dc.date.issued.fl_str_mv 2000-10-01
dc.date.accessioned.fl_str_mv 2016-01-24T12:31:11Z
dc.date.available.fl_str_mv 2016-01-24T12:31:11Z
dc.type.status.fl_str_mv info:eu-repo/semantics/publishedVersion
dc.type.driver.fl_str_mv info:eu-repo/semantics/article
format article
status_str publishedVersion
dc.identifier.citation.fl_str_mv British Journal of Pharmacology. Basingstoke: Nature Publishing Group, v. 131, n. 4, p. 788-794, 2000.
dc.identifier.uri.fl_str_mv http://repositorio.unifesp.br/handle/11600/26388
http://dx.doi.org/10.1038/sj.bjp.0703630
dc.identifier.issn.none.fl_str_mv 0007-1188
dc.identifier.doi.none.fl_str_mv 10.1038/sj.bjp.0703630
dc.identifier.wos.none.fl_str_mv WOS:000090037100020
identifier_str_mv British Journal of Pharmacology. Basingstoke: Nature Publishing Group, v. 131, n. 4, p. 788-794, 2000.
0007-1188
10.1038/sj.bjp.0703630
WOS:000090037100020
url http://repositorio.unifesp.br/handle/11600/26388
http://dx.doi.org/10.1038/sj.bjp.0703630
dc.language.iso.fl_str_mv eng
language eng
dc.relation.ispartof.none.fl_str_mv British Journal of Pharmacology
dc.rights.driver.fl_str_mv info:eu-repo/semantics/openAccess
eu_rights_str_mv openAccess
dc.format.none.fl_str_mv 788-794
dc.publisher.none.fl_str_mv Nature Publishing Group
publisher.none.fl_str_mv Nature Publishing Group
dc.source.none.fl_str_mv reponame:Repositório Institucional da UNIFESP
instname:Universidade Federal de São Paulo (UNIFESP)
instacron:UNIFESP
instname_str Universidade Federal de São Paulo (UNIFESP)
instacron_str UNIFESP
institution UNIFESP
reponame_str Repositório Institucional da UNIFESP
collection Repositório Institucional da UNIFESP
repository.name.fl_str_mv Repositório Institucional da UNIFESP - Universidade Federal de São Paulo (UNIFESP)
repository.mail.fl_str_mv
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