Cited 27 times in
Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries
DC Field | Value | Language |
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dc.contributor.author | 연수인 | - |
dc.contributor.author | 이영호 | - |
dc.contributor.author | 김주영 | - |
dc.date.accessioned | 2015-01-06T17:26:59Z | - |
dc.date.available | 2015-01-06T17:26:59Z | - |
dc.date.issued | 2014 | - |
dc.identifier.uri | https://ir.ymlib.yonsei.ac.kr/handle/22282913/100000 | - |
dc.description.abstract | 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. | - |
dc.description.statementOfResponsibility | open | - |
dc.format.extent | e110413 | - |
dc.relation.isPartOf | PLOS ONE | - |
dc.rights | CC BY-NC-ND 2.0 KR | - |
dc.rights.uri | https://creativecommons.org/licenses/by-nc-nd/2.0/kr/ | - |
dc.subject.MESH | Acetylcholine/pharmacology | - |
dc.subject.MESH | Animals | - |
dc.subject.MESH | Calcium/metabolism | - |
dc.subject.MESH | Endothelial Cells/drug effects | - |
dc.subject.MESH | Endothelial Cells/metabolism | - |
dc.subject.MESH | Mesenteric Arteries/metabolism* | - |
dc.subject.MESH | Mice | - |
dc.subject.MESH | Mice, Knockout | - |
dc.subject.MESH | Models, Animal | - |
dc.subject.MESH | Muscle, Smooth, Vascular/drug effects | - |
dc.subject.MESH | Muscle, Smooth, Vascular/metabolism | - |
dc.subject.MESH | Nitric Oxide/biosynthesis | - |
dc.subject.MESH | TRPC Cation Channels/genetics* | - |
dc.subject.MESH | TRPC Cation Channels/metabolism | - |
dc.subject.MESH | Vasoconstriction/drug effects | - |
dc.subject.MESH | Vasoconstriction/genetics* | - |
dc.subject.MESH | Vasodilation/drug effects | - |
dc.subject.MESH | Vasodilation/genetics | - |
dc.title | Transient receptor potential canonical type 3 channels control the vascular contractility of mouse mesenteric arteries | - |
dc.type | Article | - |
dc.contributor.college | College of Medicine (의과대학) | - |
dc.contributor.department | Dept. of Physiology (생리학) | - |
dc.contributor.googleauthor | Soo-In Yeon | - |
dc.contributor.googleauthor | Joo Young Kim | - |
dc.contributor.googleauthor | Dong-Soo Yeon | - |
dc.contributor.googleauthor | Joel Abramowitz | - |
dc.contributor.googleauthor | Lutz Birnbaumer | - |
dc.contributor.googleauthor | Shmuel Muallem | - |
dc.contributor.googleauthor | Young-Ho Lee | - |
dc.identifier.doi | 10.1371/journal.pone.0110413 | - |
dc.admin.author | false | - |
dc.admin.mapping | false | - |
dc.contributor.localId | A00942 | - |
dc.contributor.localId | A02350 | - |
dc.contributor.localId | A02968 | - |
dc.relation.journalcode | J02540 | - |
dc.identifier.eissn | 1932-6203 | - |
dc.identifier.pmid | 25310225 | - |
dc.contributor.alternativeName | Yeon, Soo In | - |
dc.contributor.alternativeName | Lee, Young Ho | - |
dc.contributor.alternativeName | Kim, Joo Young | - |
dc.contributor.affiliatedAuthor | Kim, Joo Young | - |
dc.contributor.affiliatedAuthor | Yeon, Soo In | - |
dc.contributor.affiliatedAuthor | Lee, Young Ho | - |
dc.citation.volume | 9 | - |
dc.citation.number | 10 | - |
dc.citation.startPage | e110413 | - |
dc.identifier.bibliographicCitation | PLOS ONE, Vol.9(10) : e110413, 2014 | - |
dc.identifier.rimsid | 54400 | - |
dc.type.rims | ART | - |
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