title: Associations of the eNOS G894T gene polymorphism with target organ damage in children with newly diagnosed primary hypertension.
abstract: BACKGROUND
  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.
  
  
  METHODS
  We 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.
  
  
  RESULTS
  Among 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).
  
  
  CONCLUSIONS
  The 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.
authors.affiliation: Department of Nephrology and Arterial Hypertension, The Children's Memorial Health Institute, Warsaw, Poland.
authors.forename: Joanna
authors.initials: J
authors.lastname: Śladowska-Kozłowska
authors.affiliation: Department of Nephrology and Arterial Hypertension, The Children's Memorial Health Institute, Warsaw, Poland. m.litwin@ipczd.pl.
authors.forename: Mieczysław
authors.initials: M
authors.lastname: Litwin
authors.affiliation: Department of Nephrology and Arterial Hypertension, The Children's Memorial Health Institute, Warsaw, Poland.
authors.forename: Anna
authors.initials: A
authors.lastname: Niemirska
authors.affiliation: Department of Biochemistry and Experimental Medicine, The Children's Memorial Health Institute, Warsaw, Poland.
authors.forename: Aldona
authors.initials: A
authors.lastname: Wierzbicka
authors.affiliation: Department of Molecular Biology, Institute of Cardiology, Warsaw, Poland.
authors.forename: Marta
authors.initials: M
authors.lastname: Roszczynko
authors.affiliation: Department of Molecular Biology, Institute of Cardiology, Warsaw, Poland.
authors.forename: Małgorzata
authors.initials: M
authors.lastname: Szperl
mesh_terms: D000293:Adolescent; D000419:Albuminuria / Q000209:etiology; D018660:Blood Pressure Monitoring, Ambulatory; D059168:Carotid Intima-Media Thickness; D002648:Child; D002675:Child, Preschool; D004452:Echocardiography; D000075222:Essential Hypertension; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D006973:Hypertension / Q000150:complications / Q000235:genetics*; D017379:Hypertrophy, Left Ventricular / Q000209:etiology; D007249:Inflammation / Q000209:etiology; D008297:Male; D052250:Nitric Oxide Synthase Type III / Q000235:genetics*; D018384:Oxidative Stress; D011110:Polymorphism, Genetic; D012307:Risk Factors
chemical_list: C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III
keywords: Children; Intima media thickness; Nitric oxide; Primary hypertension; Target organ damage; eNOS G894T gene polymorphism