Exercise training and sympathetic regulation in experimental heart failure.
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.
Zucker
Irving H
IH
Department of Physiology and Biophysics, University of Nebraska Medical Center, Nebraska Medical Center, Omaha, NE 68198-5850, USA. izucker@unmc.edu
Patel
Kaushik P
KP
Schultz
Harold D
HD
Li
Yi-Fan
YF
Wang
Wei
W
Pliquett
Rainer U
RU
D000804:Angiotensin II / Q000378:metabolism; D000818:Animals; D017704:Baroreflex / Q000502:physiology; D004195:Disease Models, Animal; D006333:Heart Failure / Q000201:enzymology / Q000378:metabolism / Q000503:physiopathology*; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D010805:Physical Conditioning, Animal / Q000502:physiology*; D011817:Rabbits; D044140:Receptor, Angiotensin, Type 1 / Q000378:metabolism; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D044140:Receptor, Angiotensin, Type 1; D000804:Angiotensin II; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase