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dc.contributor.author
Yamaguchi, Yohei
dc.contributor.author
Iribe, Gentaro
dc.contributor.author
Kaneko, Toshiyuki
dc.contributor.author
Takahashi, Ken
dc.contributor.author
Numaga-Tomita, Takuro
dc.contributor.author
Nishida, Motohiro
dc.contributor.author
Birnbaumer, Lutz
dc.contributor.author
Naruse, Keiji
dc.date.available
2018-06-07T17:56:11Z
dc.date.issued
2017-01
dc.identifier.citation
Yamaguchi, Yohei; Iribe, Gentaro; Kaneko, Toshiyuki; Takahashi, Ken; Numaga-Tomita, Takuro; et al.; TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes; Springer Tokyo; Journal Of Physiological Sciences; 68; 2; 1-2017; 153-164
dc.identifier.issn
1880-6546
dc.identifier.uri
http://hdl.handle.net/11336/47695
dc.description.abstract
When a cardiac muscle is held in a stretched position, its [Ca2+] transient increases slowly over several minutes in a process known as stress-induced slow increase in intracellular Ca2+ concentration ([Ca2+]i) (SSC). Transient receptor potential canonical (TRPC) 3 forms a non-selective cation channel regulated by the angiotensin II type 1 receptor (AT1R). In this study, we investigated the role of TRPC3 in the SSC. Isolated mouse ventricular myocytes were electrically stimulated and subjected to sustained stretch. An AT1R blocker, a phospholipase C inhibitor, and a TRPC3 inhibitor suppressed the SSC. These inhibitors also abolished the observed SSC-like slow increase in [Ca2+]i induced by angiotensin II, instead of stretch. Furthermore, the SSC was not observed in TRPC3 knockout mice. Simulation and immunohistochemical studies suggest that sarcolemmal TRPC3 is responsible for the SSC. These results indicate that sarcolemmal TRPC3, regulated by AT1R, causes the SSC.
dc.format
application/pdf
dc.language.iso
eng
dc.publisher
Springer Tokyo
dc.rights
info:eu-repo/semantics/openAccess
dc.rights.uri
https://creativecommons.org/licenses/by-nc-sa/2.5/ar/
dc.subject
Angiotensin Ii Type 1 Receptor
dc.subject
Ca2+ Handling
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Cardiomyocyte
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Mathematical Model
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Stretch
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Transient Receptor Potential Canonical 3
dc.subject.classification
Inmunología
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Medicina Básica
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CIENCIAS MÉDICAS Y DE LA SALUD
dc.title
TRPC3 participates in angiotensin II type 1 receptor-dependent stress-induced slow increase in intracellular Ca2+ concentration in mouse cardiomyocytes
dc.type
info:eu-repo/semantics/article
dc.type
info:ar-repo/semantics/artículo
dc.type
info:eu-repo/semantics/publishedVersion
dc.date.updated
2018-06-06T19:40:56Z
dc.journal.volume
68
dc.journal.number
2
dc.journal.pagination
153-164
dc.journal.pais
Japón
dc.journal.ciudad
Tokyo
dc.description.fil
Fil: Yamaguchi, Yohei. Okayama University; Japón
dc.description.fil
Fil: Iribe, Gentaro. Okayama University; Japón
dc.description.fil
Fil: Kaneko, Toshiyuki. Asahikawa Medical University; Japón
dc.description.fil
Fil: Takahashi, Ken. Okayama University; Japón
dc.description.fil
Fil: Numaga-Tomita, Takuro. National Institutes of Natural Sciences; Japón
dc.description.fil
Fil: Nishida, Motohiro. National Institutes of Natural Sciences; Japón
dc.description.fil
Fil: Birnbaumer, Lutz. Consejo Nacional de Investigaciones Científicas y Técnicas; Argentina. Research Triangle Park; Estados Unidos
dc.description.fil
Fil: Naruse, Keiji. Okayama University; Japón
dc.journal.title
Journal Of Physiological Sciences
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/doi/https://dx.doi.org/10.1007/s12576-016-0519-3
dc.relation.alternativeid
info:eu-repo/semantics/altIdentifier/url/https://link.springer.com/article/10.1007%2Fs12576-016-0519-3
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