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Assessment of Vascular Tone Responsiveness using Isolated Mesenteric Arteries with a Focus on Modulation by Perivascular Adipose Tissues
Published on: June 3, 2019
Impaired endothelium mediated vascular reactivity in endogenous Cushing's syndrome
Dinu S Chandran1, Ashok Kumar Jaryal, Viveka P Jyotsna
1Department of Physiology, All India Institute of Medical Sciences, Ansari Nagal, New Delhi, India.
Insights
Endogenous Cushing's syndrome impairs vascular reactivity and endothelial function. Elevated cortisol levels are linked to this dysfunction, increasing cardiovascular risks.
Area of Science:
- Endocrinology
- Cardiovascular Medicine
- Vascular Biology
Background:
- Endogenous Cushing's syndrome (CS) is linked to high cardiovascular morbidity and mortality.
- Multiple cardiovascular risk factors in CS likely induce endothelial dysfunction.
- Emerging evidence suggests cortisol directly contributes to vascular dysfunction in CS.
Purpose of the Study:
- To non-invasively assess vascular reactivity in CS patients.
- To investigate the association between vascular reactivity and elevated cortisol levels in CS.
- To explore the role of hypercortisolism in endothelial dysfunction in CS.
Main Methods:
- Observational study comparing 18 CS patients with 15 healthy controls.
- Non-invasive assessment of vascular reactivity using digital photoplethysmography (PPG) during reactive hyperemia (RH).
- Measured pulse wave form amplitude (PWA) and pulse transit time (PTT) changes.
Main Results:
- Maximal PWA changes during RH were significantly lower in CS patients versus controls (p=0.0079).
- Normalized PTT responses during the first minute of RH were blunted in CS patients (p=0.0425).
- PTT changes during the second minute of RH negatively correlated with morning cortisol levels (r=-0.6328, p=0.0064).
Conclusions:
- Endothelium-mediated vascular reactivity and myogenic regulation of vascular tone are impaired in CS.
- Hypercortisolism likely plays a significant role in causing impaired vascular reactivity and endothelial dysfunction in CS.
- These findings highlight potential therapeutic targets for cardiovascular risk reduction in CS.
Abstract:
Endogenous Cushing's syndrome (CS) is associated with a high incidence of cardiovascular morbidity and mortality resulting from the co-existence of multiple cardiovascular risk factors which probably induce a state of endothelial dysfunction. Recently, studies conducted in vitro as well as in normal human subjects suggest a direct role of cortisol in the causation of vascular dysfunction in this disorder. We non-invasively assessed the vascular reactivity and its potential association with elevated cortisol levels in patients of CS. A single time point observational study was conducted in 18 patients of CS and 15 age and gender matched healthy subjects. Vascular reactivity was assessed non-invasively by measuring the peripheral pulse wave form changes during reactive hyperemia (RH) using digital photoplethysmography (PPG). Parameters measured were pulse wave form amplitude (PWA), slope and pulse transit time (PTT). Maximal percentage changes in PWA during RH with reference to baseline were significantly lower in the patients as compared to controls [23.19% (13.19-53.54) vs 61.71% (38.21-95.36); p=0.0079]. Normalized PTT responses during the 1(st) minute of RH were blunted in the patients as compared to controls (1.036 ± 0.026 vs 1.056 ± 0.029; p=0.0425). Percentage changes in PTT during the 2(nd) minute of RH were negatively correlated to the morning cortisol levels in patients (r = -0.6328; p=0.0064). The present study showed that endothelium mediated vascular reactivity along with myogenic regulation of vascular tone is impaired in CS. Hypercortisolism possibly plays an important role in the causation of impaired vascular reactivity and endothelial dysfunction in CS.
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