ACE, angiotensinogen and obesity: a potential pathway leading to hypertension

J Hum Hypertens. 1997 Feb;11(2):107-11. doi: 10.1038/sj.jhh.1000391.

Abstract

The renin-angiotensin system (RAS) plays a crucial role in the regulation of fluid volume, thereby influencing blood pressure (BP). Obesity is an important risk factor for hypertension, however the physiologic basis for this relationship has not been clarified. In a population survey we examined the potential relationship between the RAS and obesity. Based on community sampling, 449 individuals were recruited from metropolitan Kingston, Jamaica. Serum angiotensin-converting enzyme (ACE) and circulating angiotensinogen levels were measured and the associated genes were typed for previously described polymorphisms. Obese individuals (body mass index > 31) had significantly higher serum ACE and angiotensinogen levels, this relationship persisted for ACE in multivariate analyses controlling for BP, hypertension status, age, and gender. The insertion/deletion polymorphism of the ACE gene was associated with variation in the levels of ACE, but inconsistently with body mass index. Variants of the angiotensinogen gene leading to amino acid substitutions at positions 174 and 235 did not influence levels either of angiotensinogen or obesity. These data suggest that obesity may alter the levels of ACE and angiotensinogen, and provide a potential pathway through which obesity leads to elevation of BP.

MeSH terms

  • Adult
  • Angiotensinogen / blood
  • Angiotensinogen / genetics*
  • Female
  • Humans
  • Hypertension / blood
  • Hypertension / etiology*
  • Male
  • Middle Aged
  • Obesity / blood
  • Obesity / complications
  • Obesity / genetics*
  • Peptidyl-Dipeptidase A / blood
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic
  • Risk Factors

Substances

  • Angiotensinogen
  • Peptidyl-Dipeptidase A