This review highlights the role of the renin-angiotensin system and oxidative stress in mediating sympathetic hyperactivation in heart failure, and how exercise training can ameliorate these effects.
Animal data link RAS-oxidative stress to CHF sympathetic activation; leaves open targeted human therapies.
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.
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Satoshi Koba (2018) studied this question.
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