Angiotensin-converting enzyme gene insertion/deletion polymorphism frequency in normotensive children with a positive family history of essential hypertension

J Paediatr Child Health. 2009 Dec;45(12):742-6. doi: 10.1111/j.1440-1754.2009.01605.x. Epub 2009 Oct 26.

Abstract

Aim: To evaluate the possible relationship between blood pressure (BP) and angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism in normotensive children with a positive family history of essential hypertension (EHT).

Material and methods: Three hundred seventy-six randomly selected normotensive schoolchildren (147 boys, 229 girls) between the ages of seven and 17 years were enrolled. Children were subdivided into a 'first-degree relative group' and a 'second-degree relative group' according to the presence of EHT in parents or grandparents, respectively. BP was measured twice from the right arm and the systolic BP, diastolic BP and mean BP were recorded. ACE gene I/D polymorphism was performed from all studied children and frequency od DD, ID and ID allele were analysed in each study group.

Results: Allelic frequencies of the DD genotype of the ACE gene were higher in children with a positive history in the first- (36.2%) and second-degree (38.3%) relatives for EHT than the controls (30.7%) (P < 0.05 for both). Children with a positive family history of EHT and a DD genotype, had significantly higher SBP, DBP and MBP levels (P < 0.05) than the children with ID or II genotypes.

Conclusion: We found that the ACE gene DD genotype was common and that BP levels were higher in Turkish children with a positive family history of EHT and DD genotype. Because the presence of DD allele might be the one of the potential contributor of EHT pathogenesis, further studies needed in large cohort for long term follow-up for EHT in children with DD allele.

MeSH terms

  • Adolescent
  • Blood Pressure Determination
  • Child
  • Female
  • Gene Deletion*
  • Gene Frequency
  • Genetic Association Studies
  • Genetic Predisposition to Disease*
  • Genotype
  • Humans
  • Hypertension / genetics*
  • Male
  • Mutagenesis, Insertional*
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Turkey

Substances

  • Peptidyl-Dipeptidase A