Abstract
BackgroundThe endothelial nitric oxide synthase (eNOS) G894T gene polymorphism is associated with the risk of primary hypertension (PH) and vascular complications in adults with PH.MethodsWe explored the associations of the G894T polymorphism with 24-h ambulatory blood pressure, left ventricular mass (LVM), carotid intima media thickness (cIMT), urinary albumin excretion, oxidative stress and inflammatory parameters in 126 children with newly diagnosed PH and in 83 healthy children.ResultsAmong the 126 children with PH 92 (73 %) had ambulatory hypertension and 34 (27 %) had severe ambulatory hypertension. Left ventricular hypertrophy (LVH) was detected in 39 (31 %) patients, cIMT of >2 standard deviation scores in 21 (16.6 %) patients, albuminuria of >30 mg/24 h in 18 (14.3 %) patients and metabolic syndrome (MS) in 22 (17.5 %) patients. The frequency of the T allele was 52.4 % in the PH group and 54.2 % in the control group (not significant), and in both groups the frequency of the T allele was consistent with the Hardy–Weinberg equilibrium. Compared with G allele carriers, hypertensive T allele carriers had increased cIMT (p < 0.05) and more severe albuminuria (not significant, p = 0.1); there was no difference between the groups in hypertension severity and LVM. T and G allele distribution did not differ between patients with and without metabolic syndrome. No significant correlations between the assessed parameters and the eNOS G894T gene polymorphism were found in the controls, although T allele carriers tended to have an increased cIMT (p = 0.09).ConclusionThe eNOS T allele is not more prevalent among hypertensive children than among healthy ones, but it is associated with early vascular damage in children with PH, independent of metabolic abnormalities. No associations between the eNOS G894T polymorphism and metabolic abnormalities were found.
Highlights
Subclinical target organ damage (TOD) in the form of left ventricular hypertrophy (LVH) and/or increased carotid intima-media thickness is already present in 30– 40 % of children with primary hypertension (PH) at the diagnosis of elevated blood pressure (BP) [1,2,3,4,5]
The main finding of our study is that the T894 allele of the endothelial nitric oxide synthase (eNOS) gene is associated with early vascular damage in children with PH independently of metabolic abnormalities
This association was not found in normotensive children
Summary
Subclinical target organ damage (TOD) in the form of left ventricular hypertrophy (LVH) and/or increased carotid intima-media thickness (cIMT) is already present in 30– 40 % of children with primary hypertension (PH) at the diagnosis of elevated blood pressure (BP) [1,2,3,4,5]. Some data indicate the involvement of endothelial nitric oxide synthase (eNOS) in the development of PH and the association of a relative or absolute decrease of eNOS activity with various vascular complications in response to hemodynamic workload [6]. The eNOS 894 T variant has lower activity and has been found to associate with coronary heart disease, carotid atherosclerosis and endothelial dysfunction [10,11,12,13,14,15,16,17] This variant is associated with enhanced vasoconstrictive response to phenylephrine, hypertensive response to endurance training and development of hypertension [13, 18, 19]. The endothelial nitric oxide synthase (eNOS) G894T gene polymorphism is associated with the risk of primary hypertension (PH) and vascular complications in adults with PH
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