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

Authors
 Soo-In Yeon  ;  Joo Young Kim  ;  Dong-Soo Yeon  ;  Joel Abramowitz  ;  Lutz Birnbaumer  ;  Shmuel Muallem  ;  Young-Ho Lee 
Citation
 PLOS ONE, Vol.9(10) : e110413, 2014 
Journal Title
 PLOS ONE 
Issue Date
2014
MeSH
Acetylcholine/pharmacology ; Animals ; Calcium/metabolism ; Endothelial Cells/drug effects ; Endothelial Cells/metabolism ; Mesenteric Arteries/metabolism* ; Mice ; Mice, Knockout ; Models, Animal ; Muscle, Smooth, Vascular/drug effects ; Muscle, Smooth, Vascular/metabolism ; Nitric Oxide/biosynthesis ; TRPC Cation Channels/genetics* ; TRPC Cation Channels/metabolism ; Vasoconstriction/drug effects ; Vasoconstriction/genetics* ; Vasodilation/drug effects ; Vasodilation/genetics
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.
Files in This Item:
T201403539.pdf Download
DOI
10.1371/journal.pone.0110413
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
1. College of Medicine (의과대학) > Dept. of Pharmacology (약리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Joo Young(김주영) ORCID logo https://orcid.org/0000-0003-2623-1491
Yeon, Soo In(연수인)
Lee, Young Ho(이영호) ORCID logo https://orcid.org/0000-0002-5749-1045
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/100000
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