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Assessing Endothelial Vasodilator Function with the Endo-PAT 2000
Published on: October 15, 2010
Endothelial dysfunction and alteration of nitric oxide/ cyclic GMP pathway in patients with exercise-induced
Hyuk Jae Chang1, Jae Hoon Chung, Byoung Joo Choi
1Dr. Hyuk-Jae Chang, Department of Cardiology, Ajou University School of Medicine, San 5 Won chon-dong, Paldal-gu, Suwon 442-721, Korea. hjchang70@hotmail.com
Insights
Exercise-induced hypertension is linked to impaired endothelial function and nitric oxide pathway dysfunction. This suggests a role for endothelial dysfunction in the cardiovascular risks associated with exercise hypertension.
Area of Science:
- Cardiovascular Physiology
- Endothelial Function Research
- Hypertension Studies
Background:
- Exaggerated blood pressure response to exercise has unclear diagnostic and prognostic implications.
- Endothelial dysfunction is a known risk factor for cardiovascular disease, but its role in exercise-induced hypertension is not well understood.
Purpose of the Study:
- To evaluate endothelial function in individuals with exercise-induced hypertension.
- To investigate the relationship between endothelial dysfunction and the nitric oxide/cyclic guanosine monophosphate (GMP) pathway in this patient group.
Main Methods:
- Assessed brachial artery endothelial function using high-resolution ultrasound in 35 patients with exercise-induced hypertension and 35 matched controls.
- Measured nitric oxide metabolites (NO2-/NO3-) and cyclic GMP levels at rest, during maximal exercise, and during recovery.
Main Results:
- Endothelial-dependent vasodilation was significantly impaired in patients with exercise-induced hypertension compared to controls.
- Impaired vasodilation correlated with age and systolic blood pressure difference during exercise.
- While NO2-/NO3- levels increased similarly in both groups during exercise, cyclic GMP levels were significantly lower in the hypertensive group during maximal exercise.
Conclusions:
- Patients with exercise-induced hypertension exhibit impaired endothelium-dependent vasodilation.
- This impairment is associated with a dysfunction in the nitric oxide/cyclic GMP pathway.
- These findings suggest that endothelial dysfunction may contribute to elevated blood pressure during exercise due to inadequate peripheral vascular adjustment.
Abstract:
The diagnostic and prognostic implication of exaggerated blood pressure response to exercise have been controversial, with opinions ranging from a benign process to a harbinger of potential cardiovascular morbidity. Endothelial dysfunction has been demonstrated in patients with atherosclerosis and as a risk factor for coronary artery disease. However, whether the cause of exercise-induced hypertension might be related to endothelial dysfunction has not been well elucidated. We evaluated endothelial function in patients who showed a systolic blood pressure > or = 210 mmHg in males and > or = 190 mmHg in females during treadmill exercise test. We measured the endothelial function of the brachial artery in 35 patients with exercise-induced hypertension, and in 35 age- and gender-matched normal control subjects, by a high resolution ultrasound technique, and the concentration of NO2-/NO3- and cyclic guanosine monophosphate (GMP). Endothelial-dependent vasodilation was impaired in patients with hypertension compared to normal controls (3.14 +/- 0.61 vs. 6.5 +/- 0.76%, p < 0.05). The extent of vasodilation was significantly correlated with age (r=-0.28, p < 0.05) and systolic blood pressure difference (r=-0.36, p < 0.05). The levels of NO2-/NO3- and cyclic GMP at maximal exercise were significantly higher than those at rest and recovery in both controls and the hypertensive group (p < 0.05). Although there was no significant difference in the increment of NO2-/NO3- during maximal exercise between the controls and hypertensive group (55 +/- 17 vs. 56 +/- 12 micro mol/L, p=NS), cyclic GMP level during maximal exercise was significantly higher in the control group than the hypertensive group (10 +/- 1.8 vs. 8.3 +/- 2.5 pmol/ml, p 0.05). Patients with exercise-induced hypertension have poor endothelium-dependent vasodilation due to an impaired nitric oxide/cyclic GMP pathway, which may play a significant role in increasing blood pressure during exercise with inadequate peripheral adjustment to changing cardiac output.
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