Evaluation of functional molecules involved in the generation and propagation of automatic activity in the pulmonary vein myocardium with three dimensional spatial imaging.
Project/Area Number |
17K08607
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
General pharmacology
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Research Institution | Toho University |
Principal Investigator |
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Project Period (FY) |
2017-04-01 – 2020-03-31
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Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2019: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2018: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
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Keywords | 薬理学 / 肺静脈心筋 / イメージング / 自動能 / 心房細動 / 3次元イメージング / 三次元イメージング |
Outline of Final Research Achievements |
We recorded the spontaneous automaticity from the myocardial layer of isolated pulmonary veins with high-speed 3-dimensional confocal microscopy and glass microelectrode technique. Spontaneous automaticity was observed in isolated pulmonary vein preparations and firing frequency was enhanced by angiotensinⅡ, while reduced by losartan, AT1 receptor blocker. AngiotensinⅡ affected the diastolic depolarization slope and induced local calcium oscillations followed by spontaneous automaticity. These results indicated that spontaneous automaticity of the pulmonary vein myocardium is influenced by the renin-angiotensin system.
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Academic Significance and Societal Importance of the Research Achievements |
心房細動は心房が高頻度で不規則に細かく震える不整脈であり、我が国には約130万人の患者が存在するといわれている。本研究は心房細動の発生源として重要視されている肺静脈の電気的自発活動に焦点を当て、自発活動の発生および伝播機序を解明することを目的とした。本研究によって、renin-angiotensin系の活性本体であるangiotensin II が肺静脈心筋に対して急性的に作用し、心房細動の発生に関与する示唆を得た。この成果は、心臓における自動能の理解を深めるとともに、心房細動発生機序の解明および新しい治療薬開発への展開が期待でき、学術的・社会的に意義のあるものである。
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Report
(4 results)
Research Products
(75 results)
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[Journal Article] Haruna Kanae, Shogo Hamaguchi, Yumi Wakasugi, Taichi Kusakabe, Keisuke Kato, Iyuki Namekata, Hikaru Tanaka. Pathological prolongation of action potential duration as a cause of the reduced alpha-adrenoceptor-mediated negative inotropy in streptozotocin-induced diabetic mice myocardium.2017
Author(s)
Haruna Kanae, Shogo Hamaguchi, Yumi Wakasugi, Taichi Kusakabe, Keisuke Kato, Iyuki Namekata, Hikaru Tanaka.
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Journal Title
J Pharmacol Sci.
Volume: 135(3)
Issue: 3
Pages: 131-133
DOI
Related Report
Peer Reviewed / Open Access
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[Journal Article] Cardiac overexpression of Epac1 in transgenic mice rescues lipopolysaccharide-induced cardiac dysfunction and inhibits Jak-STAT pathway.2017
Author(s)
Huiling Jin, Takayuki Fujita, Meihua Jin, Reiko Kurotani, Iyuki Namekata, Shogo Hamaguchi, Yuko Hidaka, Wenqian Cai, Kenji Suita, Yoshiki Ohnuki, Yasumasa Mototani, Kouichi Shiozawa, Rajesh Prajapati, Chen Liang, Masanari Umemura, Utako Yokoyama, Motohiko Sato, Hikaru Tanaka, Satoshi Okumura, Yoshihiro Ishikawa.
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Journal Title
J Mol Cell Cardiol.
Volume: 108
Pages: 170-180
DOI
Related Report
Peer Reviewed / Open Access / Int'l Joint Research
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