Neurogenic and sympathoexcitatory actions of NaCl in hypertension

Sean D. Stocker, Kevin D. Monahan, Kirsteen N. Browning

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


Excess dietary salt intake is a major contributing factor to the pathogenesis of salt-sensitive hypertension. Strong evidence suggests that salt-sensitive hypertension is attributed to renal dysfunction, vascular abnormalities, and activation of the sympathetic nervous system. Indeed, sympathetic nerve transections or interruption of neurotransmission in various brain centers lowers arterial blood pressure (ABP) in many salt-sensitive models. The purpose of this article is to discuss recent evidence that supports a role of plasma or cerebrospinal fluid hypernatremia as a key mediator of sympathoexcitation and elevated ABP. Both experimental and clinical studies using time-controlled sampling have documented that a diet high in salt increases plasma and cerebrospinal fluid sodium concentration. To the extent it has been tested, acute and chronic elevations in sodium concentration activates the sympathetic nervous system in animals and humans. A further understanding of how the central nervous system detects changes in plasma or cerebrospinal fluid sodium concentration may lead to new therapeutic treatment strategies in salt-sensitive hypertension.

Original languageEnglish (US)
Pages (from-to)538-546
Number of pages9
JournalCurrent Hypertension Reports
Issue number6
StatePublished - Dec 2013

All Science Journal Classification (ASJC) codes

  • Internal Medicine


Dive into the research topics of 'Neurogenic and sympathoexcitatory actions of NaCl in hypertension'. Together they form a unique fingerprint.

Cite this