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Updated: May 29, 2026

Ultrasound Assessment of Endothelial Function: A Technical Guideline of the Flow-mediated Dilation Test
Published on: April 27, 2016
How mental stress affects endothelial function
Noboru Toda1, Megumi Nakanishi-Toda
1Toyama Institute for Cardiovascular Pharmacology Research, 7-13, 1-Chome, Azuchi-machi, Chuo-ku, Osaka 541-0052, Japan. n.toda.toyama-bldg@orion.ocn.ne.jp
Insights
Mental stress impairs endothelial function, a key factor in cardiovascular disease. Lifestyle changes and stress-reducing interventions can help prevent and treat this dysfunction.
Area of Science:
- Cardiovascular Science
- Stress Physiology
- Endothelial Biology
Background:
- Mental stress is a significant contributor to cardiovascular events.
- Stress-related endothelial dysfunction is an early risk factor for severe cardiovascular disorders.
- Both acute and chronic stress negatively impact endothelial function.
Purpose of the Study:
- To review the mechanisms by which mental stress affects endothelial function.
- To explore the role of stress hormones and mediators in endothelial dysfunction.
- To identify potential interventions for stress-related endothelial dysfunction.
Main Methods:
- Literature review of studies on mental stress and endothelial function.
- Analysis of the molecular mechanisms involving stress hormones (e.g., glucocorticoids, catecholamines, endothelin-1) and cytokines.
- Examination of the effects of nitric oxide synthase (NOS) and nitric oxide (NO) pathways.
Main Results:
- Stress hormones like glucocorticoids and endothelin-1, along with pro-inflammatory cytokines, contribute to endothelial dysfunction.
- Mechanisms include reduced endothelial nitric oxide synthase (eNOS) expression/activity and increased NO degradation.
- While catecholamines can impair function with sustained hypertension, endogenous opioids show protective effects.
Conclusions:
- Stress-induced endothelial dysfunction is mediated by hormonal and inflammatory pathways.
- Interventions targeting cortisol, endothelin-1, inflammation, and promoting positive coping mechanisms are crucial.
- Preventing and treating stress-related endothelial dysfunction can mitigate cardiovascular disease risk.
Abstract:
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.
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