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 cental 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.
- Brain renin-angiotension system
- Central autonomic control
- Myocardial infarction
- Sympathetic nervous system
ASJC Scopus subject areas