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HERO ID
2833835
Reference Type
Journal Article
Subtype
Review
Title
Modulation of angiotensin II signaling following exercise training in heart failure
Author(s)
Zucker, IH; Schultz, HD; Patel, KP; Wang, H
Year
2015
Is Peer Reviewed?
Yes
Journal
American Journal of Physiology: Heart and Circulatory Physiology
ISSN:
0363-6135
EISSN:
1522-1539
Volume
308
Issue
8
Page Numbers
H781-H791
Language
English
PMID
25681422
DOI
10.1152/ajpheart.00026.2015
Web of Science Id
WOS:000353069400001
Abstract
Sympathetic activation is a consistent finding in the chronic heart failure (CHF) state. Current therapy for CHF targets the renin-angiotensin II (ANG II) and adrenergic systems. Angiotensin converting enzyme (ACE) inhibitors and ANG II receptor blockers are standard treatments along with β-adrenergic blockade. However, the mortality and morbidity of this disease is still extremely high, even with good medical management. Exercise training (ExT) is currently being used in many centers as an adjunctive therapy for CHF. Clinical studies have shown that ExT is a safe, effective, and inexpensive way to improve quality of life, work capacity, and longevity in patients with CHF. This review discusses the potential neural interactions between ANG II and sympatho-excitation in CHF and the modulation of this interaction by ExT. We briefly review the current understanding of the modulation of the angiotensin type 1 receptor in sympatho-excitatory areas of the brain and in the periphery (i.e., in the carotid body and skeletal muscle). We discuss possible cellular mechanisms by which ExT may impact the sympatho-excitatory process by reducing oxidative stress, increasing nitric oxide. and reducing ANG II. We also discuss the potential role of ACE2 and Ang 1-7 in the sympathetic response to ExT. Fruitful areas of further investigation are the role and mechanisms by which pre-sympathetic neuronal metabolic activity in response to individual bouts of exercise regulate redox mechanisms and discharge at rest in CHF and other sympatho-excitatory states.
Keywords
exercise training; heart failure; neural control; sympathetic; angiotensin II
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