title: [Influence of genetic factors on the development of target organ lesions in relation to age in diagnosis of arterial hypertension].
abstract: OBJECTIVE
  To analyze the impact of polymorphism of a group of genes encoding for endothelial function on the development of target organ lesions in arterial hypertension (AH) in relation to age.
  
  
  METHODS
  Six hundred and seventy-two AH patients (mean age 50.6 years; men 67%) were examined. Microalbuminuria (MAU) was estimated. Electrocardiography, echocardiography, and carotid ultrasonography were performed. A control group comprised 184 subjects. Single-nucleotide substitutions genotyping of the Glu298Asp endothelial NO synthase (eNOS), p22phox of NADPH oxidase subunit C242T, and angiotensin II type 1 receptor (ATR1) A1166C gene polymorphisms was conducted by a polymerase chain reaction (PCR) via restriction fragment length polymorphism analysis, and M235T substitution genotyping of the G-6A polymorphism of the angiotensinogen gene was performed by a real-time allele-specific PCR. The impact of the polymorphisms on the development of MAU, left ventricular hypertrophy (LVH), carotid lesion was analyzed in the groups: AH was diagnosed in subjects aged less than 35 years (n = 128) or older. The ultrasound signs of carotid lesion, LVH, and MAU were revealed in 65, 39, and 10.5% of the patients with AH, respectively.
  
  
  RESULTS
  The subgroups showed differences in the distribution of polymorphisms of the study genes in relation to age at AH detection.
  
  
  CONCLUSIONS
  In patients with AH diagnosed at less than 35 years of age, pathological changes in the carotid are associated with a G allele of the Glu298Asp eNOS polymorphism (odds ratio (OR) = 2.3; p = 0.016) and with an T allele of the p22phox of NADPH oxidase subunit C242T polymorphism (OR 1.7; p = 0.049). In this age subgroup, LVH was associated with an A allele of the Glu298Asp eNOS polymorphism (OR = 1.9; p = 0.037), MAU was with an A allele of the Glu298Asp eNOS polymorphism (OR = 3.6; p = 0.02) and a C allele of the ATR1 A1166C gene polymorphism (OR = 2.6; p = 0.034).
authors.forename: T Iu
authors.initials: TIu
authors.lastname: Kuznetsova
authors.forename: D V
authors.initials: DV
authors.lastname: Gavrilov
authors.forename: L M
authors.initials: LM
authors.lastname: Samokhodskaia
authors.forename: A Iu
authors.initials: AIu
authors.lastname: Postnov
authors.forename: S A
authors.initials: SA
authors.lastname: Boĭtsov
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D000369:Aged, 80 and over; D000419:Albuminuria / Q000209:etiology / Q000235:genetics* / Q000652:urine; D002340:Carotid Artery Diseases / Q000000981:diagnostic imaging / Q000209:etiology / Q000235:genetics* / Q000473:pathology; D004452:Echocardiography; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D006973:Hypertension / Q000150:complications* / Q000235:genetics; D017379:Hypertrophy, Left Ventricular / Q000000981:diagnostic imaging / Q000209:etiology / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide; D017539:Tunica Intima / Q000000981:diagnostic imaging / Q000473:pathology; D018615:Ultrasonography, Doppler, Color; D018616:Ultrasonography, Doppler, Duplex; D044465:White People; D055815:Young Adult