Endothelial dysfunction and alteration of nitric oxide/cyclic GMP pathway in patients with exercise-induced hypertension

Hyuk Jae Chang, Jaehoon Chung, Byoung Joo Choi, Tae Young Choi, So Yeon Choi, Myeong Ho Yoon, Gyo Seung Hwang, Joon Han Shin, Seung Jea Tahk, Byung Il William Choi

Research output: Contribution to journalArticle

9 Citations (Scopus)

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 ≥ 210 mmHg in males and ≥ 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 μmol/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.

Original languageEnglish
Pages (from-to)1014-1020
Number of pages7
JournalYonsei medical journal
Volume44
Issue number6
DOIs
Publication statusPublished - 2003 Dec 30

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Cyclic GMP
Nitric Oxide
Exercise
Hypertension
Blood Pressure
Vasodilation
Exercise Test
Control Groups
Brachial Artery
Cardiac Output
Endothelium
Coronary Artery Disease
Atherosclerosis
Morbidity

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Chang, Hyuk Jae ; Chung, Jaehoon ; Choi, Byoung Joo ; Choi, Tae Young ; Choi, So Yeon ; Yoon, Myeong Ho ; Hwang, Gyo Seung ; Shin, Joon Han ; Tahk, Seung Jea ; Choi, Byung Il William. / Endothelial dysfunction and alteration of nitric oxide/cyclic GMP pathway in patients with exercise-induced hypertension. In: Yonsei medical journal. 2003 ; Vol. 44, No. 6. pp. 1014-1020.
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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 ≥ 210 mmHg in males and ≥ 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 μmol/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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Chang, HJ, Chung, J, Choi, BJ, Choi, TY, Choi, SY, Yoon, MH, Hwang, GS, Shin, JH, Tahk, SJ & Choi, BIW 2003, 'Endothelial dysfunction and alteration of nitric oxide/cyclic GMP pathway in patients with exercise-induced hypertension', Yonsei medical journal, vol. 44, no. 6, pp. 1014-1020. https://doi.org/10.3349/ymj.2003.44.6.1014

Endothelial dysfunction and alteration of nitric oxide/cyclic GMP pathway in patients with exercise-induced hypertension. / Chang, Hyuk Jae; Chung, Jaehoon; Choi, Byoung Joo; Choi, Tae Young; Choi, So Yeon; Yoon, Myeong Ho; Hwang, Gyo Seung; Shin, Joon Han; Tahk, Seung Jea; Choi, Byung Il William.

In: Yonsei medical journal, Vol. 44, No. 6, 30.12.2003, p. 1014-1020.

Research output: Contribution to journalArticle

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T1 - Endothelial dysfunction and alteration of nitric oxide/cyclic GMP pathway in patients with exercise-induced hypertension

AU - Chang, Hyuk Jae

AU - Chung, Jaehoon

AU - Choi, Byoung Joo

AU - Choi, Tae Young

AU - Choi, So Yeon

AU - Yoon, Myeong Ho

AU - Hwang, Gyo Seung

AU - Shin, Joon Han

AU - Tahk, Seung Jea

AU - Choi, Byung Il William

PY - 2003/12/30

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N2 - 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 ≥ 210 mmHg in males and ≥ 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 μmol/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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