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心力衰竭中的血管紧张素 II、氧化应激与交感神经系统亢进

Angiotensin II, Oxidative Stress, and Sympathetic Nervous System Hyperactivity in Heart Failure.

作者信息

Koba Satoshi

机构信息

Division of Integrative Physiology, Department of Physiology, School of Medicine, Tottori University Faculty of Medicine, Yonago 683-8503, Japan.

出版信息

Yonago Acta Med. 2018 Jun 18;61(2):103-109. doi: 10.33160/yam.2018.06.002. eCollection 2018 Jun.

Abstract

In congestive heart failure (CHF), sympathetic nervous system is hyperactive. This article reviews current understandings about central and peripheral neural mechanisms underlying sympathetic hyperactivation in this pathological condition. During the development of CHF, renin-angiotensin system (RAS) activities and angiotensin II-mediated oxidative stress become enhanced. Here, on the basis of findings obtained from animal studies, it is examined how RAS overactivation and oxidative stress in central and peripheral nervous systems of CHF mediate sympathetic hyperactivation. Mechanisms by which exercise training in CHF ameliorates RAS overactivation, oxidative stress and sympathetic hyperactivation are also investigated.

摘要

在充血性心力衰竭(CHF)中,交感神经系统过度活跃。本文综述了目前对这种病理状态下交感神经过度激活的中枢和外周神经机制的认识。在CHF发展过程中,肾素-血管紧张素系统(RAS)活性和血管紧张素II介导的氧化应激增强。在此,基于动物研究的结果,探讨了CHF中枢和外周神经系统中RAS过度激活和氧化应激如何介导交感神经过度激活。还研究了CHF运动训练改善RAS过度激活、氧化应激和交感神经过度激活的机制。

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