The origin of sympathetic outflow in heart failure: the roles of angiotensin II and nitric oxide.
The regulation of sympathetic nerve activity in chronic heart failure (CHF) has been an area of renewed investigation. Understanding the central mechanisms that are responsible for sympatho-excitation in this disease state may help in reducing the deleterious effects of chronic sympatho-excitation. This review will summarize our understanding of abnormal reflex control of the circulation in CHF. The roles of the arterial baroreflex, the chemoreflex, the cardiac sympathetic afferent reflex and the cardiopulmonary reflex are discussed. New experimental techniques that allow genetic manipulation of substances such as nitric oxide synthase in discrete areas of the brain aid in clarifying the role of NO in the modulation of sympathetic tone in the CHF state. Lastly, clinical implications of this work are discussed.
Zucker
Irving H
IH
Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, NE 68198-4575, USA. izucker@unmc.edu
Schultz
Harold D
HD
Li
Yi-Fan
YF
Wang
Yu
Y
Wang
Wei
W
Patel
Kaushik P
KP
D000804:Angiotensin II / Q000502:physiology*; D000818:Animals; D017704:Baroreflex; D001921:Brain / Q000473:pathology; D006333:Heart Failure / Q000473:pathology*; D006801:Humans; D008954:Models, Biological; D009569:Nitric Oxide / Q000502:physiology*; D019001:Nitric Oxide Synthase / Q000235:genetics; D010286:Paraventricular Hypothalamic Nucleus / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism
D012333:RNA, Messenger; D000804:Angiotensin II; D009569:Nitric Oxide; D019001:Nitric Oxide Synthase