Muscle mechanoreflex overactivity in hypertension: A role for centrally-derived nitric oxide

Scott A. Smith, Anna K. Leal, Megan N. Murphy, Ryan M. Downey, Masaki Mizuno

Research output: Contribution to journalArticle

14 Scopus citations

Abstract

The cardiovascular response to exercise is abnormally large in hypertension. Over the past decade, it has become clear that the exercise pressor reflex (a peripheral feed-back mechanism originating in skeletal muscle) contributes significantly to the generation of this hyper-responsiveness. Further, it has been determined that overactivity of the mechanically (muscle mechanoreflex) and chemically (muscle metaboreflex) sensitive components of the exercise pressor reflex underpin its dysfunction. Given the recent attention in the literature, this review focuses upon the aberrant function of the muscle mechanoreflex in this disease. Evidence supporting a role for the mechanoreflex in the pathogenesis of the exaggerated cardiovascular response to physical activity is highlighted. The peripheral and central mechanisms that may be responsible for mechanoreflex overactivity in hypertension are likewise discussed. Particular attention is given to emerging evidence implicating a role for centrally-derived nitric oxide in this process.

Original languageEnglish (US)
Pages (from-to)58-63
Number of pages6
JournalAutonomic Neuroscience: Basic and Clinical
Volume188
DOIs
StatePublished - Mar 1 2015

Keywords

  • Autonomic nervous system
  • Blood pressure
  • Exercise
  • Heart rate
  • Hemodynamics
  • Sympathetic activity

ASJC Scopus subject areas

  • Endocrine and Autonomic Systems
  • Clinical Neurology
  • Cellular and Molecular Neuroscience

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