Effects of smooth muscle and endothelial cells on myocardium in the pulmonary vein

2019 Fiscal Year Final Research Report

• Project/Area Number: 17K18146
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Pharmacology in pharmacy; General pharmacology
• Research Institution: Tokyo University of Pharmacy and Life Science
• Principal Investigator: Tsuneoka Yayoi 東京薬科大学, 薬学部, 助教 (50734597)
• Project Period (FY): 2017-04-01 – 2020-03-31
• Keywords: 肺静脈

Outline of Final Research Achievements

We investigated the spontaneous activity of pulmonary vein myocardium, which is the cause of the development of atrial fibrillation. Cardiomyocytes were isolated from the pulmonary vein and their Ca2+ kinetics were compared with those of atrial and ventricular muscles. The cell morphology and Ca2+ movement of the myocardium were found to be similar to that of the atrial muscle. This suggests that the cause of the spontaneous activity in the pulmonary vein myocardium is not due to cellular Ca2+ dynamics, but its low K+ current, which is the nature of the myocardium itself. We are now investigating whether the spontaneous activity of pulmonary venous myocardium is affected by endothelial cells and smooth muscle cells.

Free Research Field

薬理学

Academic Significance and Societal Importance of the Research Achievements

本研究により、心房細動に関して、肺静脈の構造という新たな視点から理解が得られる。心房細動は高齢者で罹患者が多い不整脈であり、生活習慣病とも関連が深いため今後も増加すると予想される。合併症の予防に用いられる抗血小板薬には出血のリスクがあり、心房細動そのものに有効 な治療法は外科的手術であることを考えると、発症メカニズムの解明と安全かつ体力のない高齢者にも適用可能な新規治療戦略の構築が急がれる。心房細動や肺静脈心筋に対する今までの研究とは異なる新たな視点からの理解によって、上記のような問題の解決に大きく貢献できる可能性がある。