Roles of endothelium-derived hyperpolarizing factor to reduce intimal hyperplasia

2016 Fiscal Year Final Research Report

• Project/Area Number: 25460655
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Applied pharmacology
• Research Institution: Nagoya City University
• Principal Investigator: ITOH Takeo 名古屋市立大学, 大学院医学研究科, 研究員 (70159888)
• Research Collaborator: OTSUKA Ryo
• Project Period (FY): 2013-04-01 – 2017-03-31
• Keywords: 内皮由来膜過分極因子 / 内膜肥厚 / 静脈グラフト / 動脈グラフト / 血管内皮機能障害 / アセチルコリン / 一酸化窒素 / Ca活性化K+チャネル

Outline of Final Research Achievements

Significant intimal hyperplasia was formed with loss of functions of both endothelium-derived nitric oxide (EDNO) and endothelium-derived hyperpolarizing factor (EDHF) in rabbit autologous jugular vein graft under poor distal runoff. Ezetimibe (a selective cholesterol transport inhibitor) and vildagliptin (a dipeptidyl peptidase-4 inhibitor) each in part recovered the function of EDNO (but not EDHF) and reduced intimal hyperplasia. In contrast, in rabbit autogenous carotid artery graft model, receptor-mediated, endothelium-dependent relaxation was enhanced by increased function of EDNO (but not of EDHF). The intimal thickening was minimal, suggesting that better patency of autogenous arterial graft is considered when compared with that of vein graft in aortocoronary revascularization. These results suggest that upregulation of the EDNO function could be beneficial in reducing intimal hyperplasia in both artery graft and vein graft.

Free Research Field

循環薬理学