Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries

Autores
Yeon, Soo-In; Kim, Joo Young; Yeon, Dong-Soo; Abramowitz, Joel; Birnbaumer, Lutz; Muallem, Shmuel; Lee, Young-Ho
Año de publicación
2014
Idioma
inglés
Tipo de recurso
artículo
Estado
versión publicada
Descripción
Transient receptor potential canonical type 3 (TRPC3) channels are non-selective cation channels and regulate intracellular Ca2+ concentration. We examined the role of TRPC3 channels in agonist-, membrane depolarization (high K+)-, and mechanical (pressure)-induced vasoconstriction and vasorelaxation in mouse mesenteric arteries. Vasoconstriction and vasorelaxation of endothelial cells intact mesenteric arteries were measured in TRPC3 wild-type (WT) and knockout (KO) mice. Calcium concentration ([Ca2+]) was measured in isolated arteries from TRPC3 WT and KO mice as well as in the mouse endothelial cell line bEnd.3. Nitric oxide (NO) production and nitrate/nitrite concentrations were also measured in TRPC3 WT and KO mice. Phenylephrine-induced vasoconstriction was reduced in TRPC3 KO mice when compared to that of WT mice, but neither high K+- nor pressure-induced vasoconstriction was altered in TRPC3 KO mice. Acetylcholine-induced vasorelaxation was inhibited in TRPC3 KO mice and by the selective TRPC3 blocker pyrazole-3. Acetylcholine blocked the phenylephrine-induced increase in Ca2+ ratio and then relaxation in TRPC3 WT mice but had little effect on those outcomes in KO mice. Acetylcholine evoked a Ca2+ increase in endothelial cells, which was inhibited by pyrazole-3. Acetylcholine induced increased NO release in TRPC3 WT mice, but not in KO mice. Acetylcholine also increased the nitrate/nitrite concentration in TRPC3 WT mice, but not in KO mice. The present study directly demonstrated that the TRPC3 channel is involved in agonist-induced vasoconstriction and plays important role in NO-mediated vasorelaxation of intact mesenteric arteries.
Fil: Yeon, Soo-In. Yonsei University College of Medicine; Corea del Sur
Fil: Kim, Joo Young. Yonsei University College Of Medicine; . Yonsei University College of Medicine; Corea del Sur
Fil: Yeon, Dong-Soo. Kwandong University College of Medicine; Corea del Sur
Fil: Abramowitz, Joel. National Institute of Environmental Health Sciences; Estados Unidos
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute of Environmental Health Sciences; Estados Unidos
Fil: Muallem, Shmuel. National Institutes of Health; Estados Unidos
Fil: Lee, Young-Ho. Yonsei University College of Medicine; Corea del Sur
Materia
TRPC3
mesenteric arteries.
Nivel de accesibilidad
acceso abierto
Condiciones de uso
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
Repositorio
CONICET Digital (CONICET)
Institución
Consejo Nacional de Investigaciones Científicas y Técnicas
OAI Identificador
oai:ri.conicet.gov.ar:11336/96060
Acceder
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oai_identifier_str oai:ri.conicet.gov.ar:11336/96060
network_acronym_str CONICETDig
repository_id_str 3498
network_name_str CONICET Digital (CONICET)
spelling Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteriesYeon, Soo-InKim, Joo YoungYeon, Dong-SooAbramowitz, JoelBirnbaumer, LutzMuallem, ShmuelLee, Young-HoTRPC3mesenteric arteries.https://purl.org/becyt/ford/1.6https://purl.org/becyt/ford/1Transient receptor potential canonical type 3 (TRPC3) channels are non-selective cation channels and regulate intracellular Ca2+ concentration. We examined the role of TRPC3 channels in agonist-, membrane depolarization (high K+)-, and mechanical (pressure)-induced vasoconstriction and vasorelaxation in mouse mesenteric arteries. Vasoconstriction and vasorelaxation of endothelial cells intact mesenteric arteries were measured in TRPC3 wild-type (WT) and knockout (KO) mice. Calcium concentration ([Ca2+]) was measured in isolated arteries from TRPC3 WT and KO mice as well as in the mouse endothelial cell line bEnd.3. Nitric oxide (NO) production and nitrate/nitrite concentrations were also measured in TRPC3 WT and KO mice. Phenylephrine-induced vasoconstriction was reduced in TRPC3 KO mice when compared to that of WT mice, but neither high K+- nor pressure-induced vasoconstriction was altered in TRPC3 KO mice. Acetylcholine-induced vasorelaxation was inhibited in TRPC3 KO mice and by the selective TRPC3 blocker pyrazole-3. Acetylcholine blocked the phenylephrine-induced increase in Ca2+ ratio and then relaxation in TRPC3 WT mice but had little effect on those outcomes in KO mice. Acetylcholine evoked a Ca2+ increase in endothelial cells, which was inhibited by pyrazole-3. Acetylcholine induced increased NO release in TRPC3 WT mice, but not in KO mice. Acetylcholine also increased the nitrate/nitrite concentration in TRPC3 WT mice, but not in KO mice. The present study directly demonstrated that the TRPC3 channel is involved in agonist-induced vasoconstriction and plays important role in NO-mediated vasorelaxation of intact mesenteric arteries.Fil: Yeon, Soo-In. Yonsei University College of Medicine; Corea del SurFil: Kim, Joo Young. Yonsei University College Of Medicine; . Yonsei University College of Medicine; Corea del SurFil: Yeon, Dong-Soo. Kwandong University College of Medicine; Corea del SurFil: Abramowitz, Joel. National Institute of Environmental Health Sciences; Estados UnidosFil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute of Environmental Health Sciences; Estados UnidosFil: Muallem, Shmuel. National Institutes of Health; Estados UnidosFil: Lee, Young-Ho. Yonsei University College of Medicine; Corea del SurPublic Library of Science2014-10info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionhttp://purl.org/coar/resource_type/c_6501info:ar-repo/semantics/articuloapplication/pdfapplication/pdfhttp://hdl.handle.net/11336/96060Yeon, Soo-In; Kim, Joo Young; Yeon, Dong-Soo; Abramowitz, Joel; Birnbaumer, Lutz; et al.; Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries; Public Library of Science; Plos One; 9; 10; 10-2014; 1-91932-6203CONICET DigitalCONICETenginfo:eu-repo/semantics/altIdentifier/url/https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0110413info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0110413info:eu-repo/semantics/openAccesshttps://creativecommons.org/licenses/by-nc-sa/2.5/ar/reponame:CONICET Digital (CONICET)instname:Consejo Nacional de Investigaciones Científicas y Técnicas2025-09-29T09:36:04Zoai:ri.conicet.gov.ar:11336/96060instacron:CONICETInstitucionalhttp://ri.conicet.gov.ar/Organismo científico-tecnológicoNo correspondehttp://ri.conicet.gov.ar/oai/requestdasensio@conicet.gov.ar; lcarlino@conicet.gov.arArgentinaNo correspondeNo correspondeNo correspondeopendoar:34982025-09-29 09:36:04.33CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicasfalse
dc.title.none.fl_str_mv Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
title Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
spellingShingle Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
Yeon, Soo-In
TRPC3
mesenteric arteries.
title_short Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
title_full Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
title_fullStr Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
title_full_unstemmed Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
title_sort Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
dc.creator.none.fl_str_mv Yeon, Soo-In
Kim, Joo Young
Yeon, Dong-Soo
Abramowitz, Joel
Birnbaumer, Lutz
Muallem, Shmuel
Lee, Young-Ho
author Yeon, Soo-In
author_facet Yeon, Soo-In
Kim, Joo Young
Yeon, Dong-Soo
Abramowitz, Joel
Birnbaumer, Lutz
Muallem, Shmuel
Lee, Young-Ho
author_role author
author2 Kim, Joo Young
Yeon, Dong-Soo
Abramowitz, Joel
Birnbaumer, Lutz
Muallem, Shmuel
Lee, Young-Ho
author2_role author
author
author
author
author
author
dc.subject.none.fl_str_mv TRPC3
mesenteric arteries.
topic TRPC3
mesenteric arteries.
purl_subject.fl_str_mv https://purl.org/becyt/ford/1.6
https://purl.org/becyt/ford/1
dc.description.none.fl_txt_mv Transient receptor potential canonical type 3 (TRPC3) channels are non-selective cation channels and regulate intracellular Ca2+ concentration. We examined the role of TRPC3 channels in agonist-, membrane depolarization (high K+)-, and mechanical (pressure)-induced vasoconstriction and vasorelaxation in mouse mesenteric arteries. Vasoconstriction and vasorelaxation of endothelial cells intact mesenteric arteries were measured in TRPC3 wild-type (WT) and knockout (KO) mice. Calcium concentration ([Ca2+]) was measured in isolated arteries from TRPC3 WT and KO mice as well as in the mouse endothelial cell line bEnd.3. Nitric oxide (NO) production and nitrate/nitrite concentrations were also measured in TRPC3 WT and KO mice. Phenylephrine-induced vasoconstriction was reduced in TRPC3 KO mice when compared to that of WT mice, but neither high K+- nor pressure-induced vasoconstriction was altered in TRPC3 KO mice. Acetylcholine-induced vasorelaxation was inhibited in TRPC3 KO mice and by the selective TRPC3 blocker pyrazole-3. Acetylcholine blocked the phenylephrine-induced increase in Ca2+ ratio and then relaxation in TRPC3 WT mice but had little effect on those outcomes in KO mice. Acetylcholine evoked a Ca2+ increase in endothelial cells, which was inhibited by pyrazole-3. Acetylcholine induced increased NO release in TRPC3 WT mice, but not in KO mice. Acetylcholine also increased the nitrate/nitrite concentration in TRPC3 WT mice, but not in KO mice. The present study directly demonstrated that the TRPC3 channel is involved in agonist-induced vasoconstriction and plays important role in NO-mediated vasorelaxation of intact mesenteric arteries.
Fil: Yeon, Soo-In. Yonsei University College of Medicine; Corea del Sur
Fil: Kim, Joo Young. Yonsei University College Of Medicine; . Yonsei University College of Medicine; Corea del Sur
Fil: Yeon, Dong-Soo. Kwandong University College of Medicine; Corea del Sur
Fil: Abramowitz, Joel. National Institute of Environmental Health Sciences; Estados Unidos
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. National Institute of Environmental Health Sciences; Estados Unidos
Fil: Muallem, Shmuel. National Institutes of Health; Estados Unidos
Fil: Lee, Young-Ho. Yonsei University College of Medicine; Corea del Sur
description Transient receptor potential canonical type 3 (TRPC3) channels are non-selective cation channels and regulate intracellular Ca2+ concentration. We examined the role of TRPC3 channels in agonist-, membrane depolarization (high K+)-, and mechanical (pressure)-induced vasoconstriction and vasorelaxation in mouse mesenteric arteries. Vasoconstriction and vasorelaxation of endothelial cells intact mesenteric arteries were measured in TRPC3 wild-type (WT) and knockout (KO) mice. Calcium concentration ([Ca2+]) was measured in isolated arteries from TRPC3 WT and KO mice as well as in the mouse endothelial cell line bEnd.3. Nitric oxide (NO) production and nitrate/nitrite concentrations were also measured in TRPC3 WT and KO mice. Phenylephrine-induced vasoconstriction was reduced in TRPC3 KO mice when compared to that of WT mice, but neither high K+- nor pressure-induced vasoconstriction was altered in TRPC3 KO mice. Acetylcholine-induced vasorelaxation was inhibited in TRPC3 KO mice and by the selective TRPC3 blocker pyrazole-3. Acetylcholine blocked the phenylephrine-induced increase in Ca2+ ratio and then relaxation in TRPC3 WT mice but had little effect on those outcomes in KO mice. Acetylcholine evoked a Ca2+ increase in endothelial cells, which was inhibited by pyrazole-3. Acetylcholine induced increased NO release in TRPC3 WT mice, but not in KO mice. Acetylcholine also increased the nitrate/nitrite concentration in TRPC3 WT mice, but not in KO mice. The present study directly demonstrated that the TRPC3 channel is involved in agonist-induced vasoconstriction and plays important role in NO-mediated vasorelaxation of intact mesenteric arteries.
publishDate 2014
dc.date.none.fl_str_mv 2014-10
dc.type.none.fl_str_mv info:eu-repo/semantics/article
info:eu-repo/semantics/publishedVersion
http://purl.org/coar/resource_type/c_6501
info:ar-repo/semantics/articulo
format article
status_str publishedVersion
dc.identifier.none.fl_str_mv http://hdl.handle.net/11336/96060
Yeon, Soo-In; Kim, Joo Young; Yeon, Dong-Soo; Abramowitz, Joel; Birnbaumer, Lutz; et al.; Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries; Public Library of Science; Plos One; 9; 10; 10-2014; 1-9
1932-6203
CONICET Digital
CONICET
url http://hdl.handle.net/11336/96060
identifier_str_mv Yeon, Soo-In; Kim, Joo Young; Yeon, Dong-Soo; Abramowitz, Joel; Birnbaumer, Lutz; et al.; Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries; Public Library of Science; Plos One; 9; 10; 10-2014; 1-9
1932-6203
CONICET Digital
CONICET
dc.language.none.fl_str_mv eng
language eng
dc.relation.none.fl_str_mv info:eu-repo/semantics/altIdentifier/url/https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0110413
info:eu-repo/semantics/altIdentifier/doi/10.1371/journal.pone.0110413
dc.rights.none.fl_str_mv info:eu-repo/semantics/openAccess
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
eu_rights_str_mv openAccess
rights_invalid_str_mv https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.format.none.fl_str_mv application/pdf
application/pdf
dc.publisher.none.fl_str_mv Public Library of Science
publisher.none.fl_str_mv Public Library of Science
dc.source.none.fl_str_mv reponame:CONICET Digital (CONICET)
instname:Consejo Nacional de Investigaciones Científicas y Técnicas
reponame_str CONICET Digital (CONICET)
collection CONICET Digital (CONICET)
instname_str Consejo Nacional de Investigaciones Científicas y Técnicas
repository.name.fl_str_mv CONICET Digital (CONICET) - Consejo Nacional de Investigaciones Científicas y Técnicas
repository.mail.fl_str_mv dasensio@conicet.gov.ar; lcarlino@conicet.gov.ar
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score 13.070432

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