title: Endothelial dysfunction and alteration of nitric oxide/ cyclic GMP pathway in patients with exercise-induced hypertension.
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.
authors.affiliation: Dr. 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
authors.forename: Hyuk Jae
authors.initials: HJ
authors.lastname: Chang
authors.forename: Jae Hoon
authors.initials: JH
authors.lastname: Chung
authors.forename: Byoung Joo
authors.initials: BJ
authors.lastname: Choi
authors.forename: Tae Young
authors.initials: TY
authors.lastname: Choi
authors.forename: So Yeon
authors.initials: SY
authors.lastname: Choi
authors.forename: Myeong Ho
authors.initials: MH
authors.lastname: Yoon
authors.forename: Gyo Seung
authors.initials: GS
authors.lastname: Hwang
authors.forename: Joon Han
authors.initials: JH
authors.lastname: Shin
authors.forename: Seung Jea
authors.initials: SJ
authors.lastname: Tahk
authors.forename: Byung-Il William
authors.initials: BI
authors.lastname: Choi
mesh_terms: D000328:Adult; D006152:Cyclic GMP / Q000378:metabolism*; D004730:Endothelium, Vascular / Q000503:physiopathology*; D015444:Exercise; D005260:Female; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology*; D008297:Male; D008875:Middle Aged; D009569:Nitric Oxide / Q000378:metabolism*
chemical_list: D009569:Nitric Oxide; D006152:Cyclic GMP