Modifications to central neural circuitry during heart failure.
OBJECTIVE
During heart failure (HF), excess sodium retention is triggered by increased plasma renin-angiotensin-aldosterone activity and increased basal sympathetic nerve discharge (SND). Enhanced basal SND in the renal nerves plays a role in sodium retention. Therefore, as a hypothetical model for the central sympathetic control pathways that are dysregulated as a consequence of HF, the central neural pathways regulating the sympathetic motor output to the kidney are reviewed in the context of their role during HF.


CONCLUSIONS
From these findings, a model of the neuroanatomical circuitry that may be affected during HF is constructed.
Weiss
M L
ML
Department of Anatomy and Physiology, Kansas State University, 1600 Denison Avenue, Manhattan, KS 66506-5602, USA.
Kenney
M J
MJ
Musch
T I
TI
Patel
K P
KP
D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology*; D001921:Brain / Q000503:physiopathology*; D002303:Cardiac Output, Low / Q000503:physiopathology*; D004525:Efferent Pathways / Q000502:physiology; D005728:Ganglia, Sympathetic / Q000503:physiopathology; D006801:Humans; D007668:Kidney / Q000294:innervation / Q000503:physiopathology; D009474:Neurons / Q000502:physiology; D018377:Neurotransmitter Agents / Q000502:physiology; D010286:Paraventricular Hypothalamic Nucleus / Q000503:physiopathology; D051381:Rats; D012084:Renin-Angiotensin System / Q000502:physiology*; D013564:Sympathetic Nervous System / Q000503:physiopathology
D018377:Neurotransmitter Agents