Sympathetic activation in heart failure: Elucidation of a novel framework and the control mechanisms

2016 Fiscal Year Final Research Report

• Project/Area Number: 24390198
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Circulatory organs internal medicine
• Research Institution: Kyushu University
• Principal Investigator: Hirooka Yoshitaka 九州大学, 循環器病未来医療研究センター, 教授 (90284497)
• Co-Investigator(Kenkyū-buntansha): 井手 友美 九州大学, 医学(系)研究科(研究院), 講師 (90380625) ; 岸 拓弥 九州大学, 循環器病未来医療研究センター, 准教授 (70423514) ; 伊藤 浩司 九州大学, 医学(系)研究科(研究院), 共同研究員 (10452757)
• Project Period (FY): 2012-04-01 – 2017-03-31
• Keywords: 血圧 / 心不全 / 交感神経系 / 脳 / レニン－アンジオテンシン系 / 慢性炎症 / 免疫系

Outline of Final Research Achievements

We investigated mechanisms involved in the regulation of sympathetic activation in heart failure The findings are as follows. Alteration of innate immunity and immune cells proportion contribute to sympathetic activation. Activation of astrocytes and microglia play a role in activation of the sympathetic nervous system. Renal denervation attenuated enhanced sympathetic drive via inhibition of hypothalamic activity. Cardiac sympathetic afferent reflex plays an important role in the progression of cardiac hypertrophy during the phase of pressure overload. As an initial step of heart failure, epithelial Na channel activation in the hypothalamus contributes to blood pressure elevation resulted from acquired salt sensitivity. These findings support a novel framework including neural, humoral, cytokines and other cell factors.

Free Research Field

内科系臨床医学・循環器内科学