M L Weiss1, M J Kenney, T I Musch, K P Patel. 1. Department of Anatomy and Physiology, Kansas State University, 1600 Denison Avenue, Manhattan, KS 66506-5602, USA.
Abstract
AIM: 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. CONCLUSION: From these findings, a model of the neuroanatomical circuitry that may be affected during HF is constructed.
AIM: 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. CONCLUSION: From these findings, a model of the neuroanatomical circuitry that may be affected during HF is constructed.
Authors: David W Infanger; Xian Cao; Scott D Butler; Melissa A Burmeister; Yi Zhou; John A Stupinski; Ram V Sharma; Robin L Davisson Journal: Circ Res Date: 2010-04-22 Impact factor: 17.367