Pathophysiological role of kidney in systemic oxidative stress during chronic intermittent hypoxia.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09297
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Kidney internal medicine
• Research Institution: Juntendo University
• Principal Investigator: KOBAYASHI TAKASHI 順天堂大学, 医学部, 助教 (70459056)
• Co-Investigator(Kenkyū-buntansha): 菅谷 健 順天堂大学, 医学部, 非常勤講師 (40381561) ; 富野 康日己 順天堂大学, 医学部, 名誉教授 (60130077) ; 鈴木 祐介 順天堂大学, 医学(系)研究科(研究院), 教授 (70372935)
• Research Collaborator: TAKAHASHI Keiko 順天堂大学, 腎臓内科, 非常勤助手
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 酸化ストレス / 睡眠時無呼吸症候群 / 間欠的低酸素 / 腎交感神経 / 高血圧 / レニンアンギオテンシン / L-FABP

Outline of Final Research Achievements

Present study demonstrated that chronic intermittent hypoxia (CIH) -mediated renal sympathetic nerve activation is involved in increased systemic oxidative stress, renin angiotensin system (RAS) activation, and endothelial dysfunction, and therefore contributing to the development of hypertension. These deleterious effects by CIH were completely blocked by renal denervation (RD) treatment. On the other hand, Liver-type fatty acid-binding protein (L-FABP) overexpression markedly reduced systemic oxidative stress, while RAS and blood pressure levels were not altered in this model during the observation periods.
RD as well as L-FABP overexpression could be a novel therapeutic strategy to prevent the development of hypertension and ameliorate oxidative stress in patients with SAS.

Free Research Field

酸化ストレス