Alteration of Nitric Oxide/cyclic-GMP pathway in patients with exaggerated systolic blood pressure response during exercise test

Park, In Whee; Chang, Hyuk Jae; Chung, Jaehoon; Shin, Joon Han; Choi, Tae Young; Choi, So Yeon; Yoon, Myung Ho; Hwang, Gyo Seung; Tahk, Seung Jae; Choi, Byung Il William

Abstract

BACKGROUND: The diagnostic and prognostic implication of exaggerated blood pressure response to exercise has not been well characterized. Endothelial dysfunction has been demonstrated in patients with atherosclerosis or with risk factors for coronary artery disease. However, whether the cause of exercise induced hypertension might be due to endothelial dysfunction has not been well elucidated. Therefore, we designed this study to evaluate the endothelial function in patients with exaggerated blood pressure response during exercise.
METHODS
Exercise hypertension is defined as a systolic blood pressure >or= 210 mmHg in men and >or= 190 mmHg in female, during treadmill exercise test. The endothelial function of the brachial artery, in 35 patients with exercise hypertension and 35 control subjects (mean age of 45.5+/-8.1) were measured by a high resolution ultrasound technique. The concentrations of nitrite and cyclic-GMP were measured from exercise hypertension group and control subjects during, before and after treadmill exercise.
RESULTS
There were no significant differences in the clinical variables between the control and exercise hypertension group. The LVH on ECG was detected more frequently in exercise hypertension group (14 % vs. 40 %, p<0.05) and LV mass/BSA (132+/-12 vs. 139+/-14 g/m2, p<0.05) was also higher in exercise hypetension group. Endothelial-dependent vasodilation was impaired in patients with exercise hypertension (6.5+/-0.8 vs. 3.1+/-0.6 %, p<0.05). On univariate analysis, the extent of vasodilation was significantly correlated with age (r=-0.28, p<0.05) and delta systolic blood pressure (r=-0.36, p<0.05). Both the levels of NO2-/NO3- and cyclic-GMP at the maximal exercise were significantly higher than those at rest and recovery in control and exercise hypertension group (p<0.05). Although there was no difference at the increment of NO2-/NO3- during the maximal exercise between the control and exercise hypertension group (55+/-17 vs. 56+/-12 mmHg, p>0.05), a significant difference of cyclic GMP level during the maximal exercise was noted between the groups (10+/-1.8 vs. 8.3+/-2.5 pmol/mL, p<0.05). CONCLSUION: Patients with exercise induced hypertension have impaired endothelium-dependent vasodilation. This study supports the concept that endothelial dysfunction may play a significant role in exercise induced hypertension.