Modifications to central neural circuitry during heart failure

M. L. Weiss, M. J. Kenney, T. I. Musch, K. P. Patel

Research output: Contribution to journalArticle

19 Scopus citations

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 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.

Original languageEnglish (US)
Pages (from-to)57-67
Number of pages11
JournalActa Physiologica Scandinavica
Volume177
Issue number1
DOIs
Publication statusPublished - Jan 18 2003

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Keywords

  • Brain renin-angiotension system
  • Central autonomic control
  • Kidney
  • Myocardial infarction
  • Sympathetic nervous system

ASJC Scopus subject areas

  • Physiology

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