Alpha-2 adrenoceptors are present in rat aorta smooth muscle cells, and their action is mediated by ATP-sensitive K+ channels
Autor(a) principal: | |
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Data de Publicação: | 2000 |
Outros Autores: | , , |
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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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 |
|
_version_ |
1802764170834214912 |