High sodium intake strengthens the association of ACE I/D polymorphism with blood pressure in a community

Am J Hypertens. 2007 Jul;20(7):751-7. doi: 10.1016/j.amjhyper.2007.01.018.

Abstract

Background: Limited evidence is available on a gene-environment interaction of angiotensin-converting enzyme (ACE) gene I/D polymorphism and high blood pressure (BP) with salt intake among general populations. We hypothesized that persons with the I allele of the ACE gene have elevated BP levels in response to a higher sodium intake, and thus the association of ACE I/D polymorphism with BP levels was stronger among persons with a higher sodium intake than those with a lower sodium intake.

Methods: We conducted a population-based cross-sectional study of 2823 men and women aged 30 to 74 years in a Japanese rural community to examine the association of the ACE I/D polymorphism with BP levels stratified by salt intake, as estimated by 24-h urine collection and dietary questionnaire. Polymorphism of the ACE I/D was detected by an allele-specific polymerase chain reaction.

Results: There was no significant difference in BP levels among DD, ID, and II groups for either sex or total samples. However, mean difference in diastolic BP levels for II versus DD groups was +3.0 mm Hg (P = .003) among persons with higher sodium excretion, +1.8 mm Hg (P = .04) among those with higher present sodium intake score, and +1.7 mm Hg (P = .06) among those with higher past sodium intake score.

Conclusions: A high sodium intake strengthens the association of ACE I/D polymorphism with BP levels in community-based samples.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Aged
  • Alleles
  • Asian People / genetics
  • Blood Pressure / drug effects*
  • Blood Pressure / genetics
  • Cross-Sectional Studies
  • Female
  • Humans
  • Introns
  • Japan
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic
  • Sodium, Dietary / pharmacology*

Substances

  • Sodium, Dietary
  • Peptidyl-Dipeptidase A