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Updated: Jun 21, 2026

Evaluation of the Cognitive Performance of Hypertensive Patients with Silent Cerebrovascular Lesions
Published on: April 23, 2021
Cerebrovascular mental stress reactivity is impaired in hypertension
Tasneem Z Naqvi1, Hanh K Hyuhn
1Division of Cardiology at Cedars Sinai Heart Institute, Cedars-Sinai Medical Center, University of Southern California, Los Angeles, CA, USA. tnaqvi@usc.edu
Insights
Mental stress causes carotid artery vasodilation in healthy individuals, but this response is blunted in hypertension, suggesting cerebral vascular endothelial dysfunction. This study highlights a novel ultrasound method for assessing hypertension
Area of Science:
- Cardiovascular physiology
- Cerebrovascular research
- Hypertension studies
Background:
- Brachial artery reactivity is impaired in hypertension.
- Endothelial dysfunction is generalized in hypertensive individuals.
- Carotid artery (CA) reactivity may also be affected by hypertension.
Purpose of the Study:
- To compare CA endothelium-dependent vasodilation in response to mental stress in normal and hypertensive subjects.
Main Methods:
- Evaluated CA reactivity to mental stress in young healthy volunteers, older healthy volunteers, and patients with essential hypertension.
- Utilized transcranial Doppler ultrasound to measure middle cerebral artery (MCA) blood flow before and after mental stress in a subset of participants.
Main Results:
- Mental stress induced CA vasodilation and increased CA and MCA blood flow in healthy subjects (young and old).
- Hypertensive subjects showed no significant CA vasodilation or increase in CA blood flow in response to mental stress.
- No difference in CA response to nitroglycerin was observed between healthy and hypertensive subjects, indicating preserved smooth muscle function.
Conclusions:
- Mental stress induces CA vasodilation and enhances cerebral blood flow in healthy individuals.
- This response is attenuated in hypertensive subjects, suggesting impaired cerebrovascular endothelial function.
- Ultrasound assessment of mental stress-induced CA reactivity is a novel method to evaluate hypertension's impact on cerebrovascular function and blood flow reserve.
Background:
Brachial artery reactivity in response to shear stress is altered in subjects with hypertension. Since endothelial dysfunction is generalized, we hypothesized that carotid artery (CA) reactivity would also be altered in hypertension.
Purpose:
To compare (CA endothelium-dependent vasodilation in response to mental stress in normal and hypertensive subjects.
Methods:
We evaluated CA reactivity to mental stress in 10 young healthy human volunteers (aged 23 +/- 4 years), 20 older healthy volunteers (aged 49 +/- 11 years) and in 28 patients with essential hypertension (aged 51 +/- 13 years). In 10 healthy volunteers and 12 hypertensive subjects, middle cerebral artery (MCA) PW transcranial Doppler was performed before and 3 minutes after mental stress.
Results:
Mental stress by Stroop color word conflict, math or anger recall tests caused CA vasodilation in young healthy subjects (0.61 +/- 0.06 to 0.65 +/- 0.07 cm, p < 0.05) and in older healthy subjects (0.63 +/- 0.06 to 0.66 +/- 0.07 cm, p < 0.05), whereas no CA vasodilation occurred in hypertensive subjects (0.69 +/- 0.06 to 0.68 +/- 0.07 cm; p, NS). CA blood flow in response to mental stress increased in young healthy subjects (419 +/- 134 to 541 +/- 209 ml, p < 0.01 vs. baseline) and in older healthy subjects (351 +/- 114 to 454 +/- 136 ml, p < 0.01 vs. baseline) whereas no change in blood flow (444 +/- 143 vs. 458 +/- 195 ml; p, 0.59) occurred in hypertensive subjects. There was no difference in the CA response to nitroglycerin in healthy and hypertensive subjects. Mental stress caused a significant increase in baseline to peak MCA systolic (84 +/- 22 to 95 +/- 22 cm/s, p < 0.05), diastolic (42 +/- 12 to 49 +/- 14 cm/s, p < 0.05) as well as mean (30 +/- 13 to 39 +/- 13 cm/s, p < 0.05) PW Doppler velocities in normal subjects, whereas no change in systolic (70 +/- 18 to 73 +/- 22 cm/s, p < 0.05), diastolic (34 +/- 14 to 37 +/- 14 cm/s, p = ns) or mean velocities (25 +/- 9 to 26 +/- 9 cm/s, p = ns) occurred in hypertensive subjects, despite a similar increase in heart rate and blood pressure in response to mental stress in both groups.
Conclusion:
Mental stress produces CA vasodilation and is accompanied by an increase in CA and MCA blood flow in healthy subjects. This mental stress induced CA vasodilation and flow reserve is attenuated in subjects with hypertension and may reflect cerebral vascular endothelial dysfunction. Assessment of mental stress induced CA reactivity by ultrasound is a novel method for assessing the impact of hypertension on cerebrovascular endothelial function and blood flow reserve.
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