How mental stress affects endothelial function

Pflugers Arch. 2011 Dec;462(6):779-94. doi: 10.1007/s00424-011-1022-6. Epub 2011 Sep 23.


Mental stress is an important factor contributing to recognized mechanisms underlying cardiovascular events. Among these, stress-related endothelial dysfunction is an early risk factor that predicts future development of severe cardiovascular disorders. Acute mental stress by a variety of tests impairs endothelial function in humans, although the opposite results have been reported by some investigators. Chronic stress always deteriorates endothelial function in humans and experimental animals. Stress hormones, such as glucocorticoids and pro-inflammatory cytokines, and endothelin-1 liberated in response to mental stress participate in endothelial dysfunction possibly via downregulation of endothelial nitric oxide synthase (eNOS) expression, eNOS inactivation, decreased nitric oxide (NO) actions, and increased NO degradation, together with vasoconstriction counteracting against NO-induced vasodilatation. Catecholamines do not directly affect endothelial function but impair its function when blood pressure elevation by the amines is sustained. Endogenous opioids favorably affect endothelial function, which counteract deteriorating effects of other stress hormones and mediators. Inhibition of cortisol and endothelin-1 production, prevention of pro-inflammatory mediator accumulation, hypnotics, mirthful laughter, humor orientation, and lifestyle modification would contribute to the prevention and treatment for stress-related endothelial dysfunction and future serious cardiovascular disease.

Publication types

  • Review

MeSH terms

  • Animals
  • Cardiovascular Diseases / etiology*
  • Cardiovascular Diseases / physiopathology*
  • Catecholamines / metabolism
  • Cytokines / metabolism
  • Endothelin-1 / metabolism
  • Endothelium, Vascular / physiology*
  • Humans
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase Type III / metabolism
  • Opioid Peptides / metabolism
  • Risk Factors
  • Stress, Psychological / complications*


  • Catecholamines
  • Cytokines
  • Endothelin-1
  • Opioid Peptides
  • Nitric Oxide
  • Nitric Oxide Synthase Type III