Role of paraventricular nucleus in mediating sympathetic outflow in heart failure

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A number of neurohumoral processes are activated in heart failure, including an increase in the plasma concentration of norepinephrine. Few studies have been performed to examine the role of the central nervous system in the activation of sympathetic outflow during heart failure (HF). In this paper I review these limited studies, with particular emphasis on examining the role of the paraventricular nucleus (PVN) in the exaggerated sympathetic outflow commonly observed in heart failure. The conclusion is that heart failure is associated with changes in specific areas in the brain and that alterations in the activation of neurons in the PVN are likely related to abnormalities in vasopressin production, blood volume regulation, and sympathoexcitation observed in the heart failure state. Furthermore, neuronal nitric oxide within the PVN that is involved in mediating sympathetic outflow via a GABA mechanism from the PVN may be deficient in inhibiting overall sympathetic outflow leading to the exaggerated sympathetic outflow commonly observed in heart failure.

Original languageEnglish (US)
Pages (from-to)73-86
Number of pages14
JournalHeart Failure Reviews
Issue number1
Publication statusPublished - May 29 2000



  • GABA
  • Nitric oxide
  • Paraventricular nucleus
  • Sympathetic nerve activity

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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