In this review, we put forth the hypothesis that reduction in sympathetic outflow after exercise training of animals with heart failure is mediated by reductions in angiotensin II and in angiotensin type 1 receptors. Furthermore, we provide evidence that exercise training provides for an upregulation of the neuronal isoform of nitric oxide synthase in the central nervous system that is sympathoinhibitory.
- Angiotensin II
- Myocardial infarction
- Nitric oxide synthase
ASJC Scopus subject areas
- Orthopedics and Sports Medicine
- Physical Therapy, Sports Therapy and Rehabilitation