Polymorphism of the angiotensin I converting enzyme gene is apparently not related to high blood pressure: Dutch Hypertension and Offspring Study

J Hypertens. 1993 Apr;11(4):345-8. doi: 10.1097/00004872-199304000-00003.


Objective: Studies in genetically hypertensive rats and their normotensive Wistar-Kyoto control rats have revealed a linkage of a chromosomal region containing the angiotensin converting enzyme (ACE) gene with blood pressure. This led to the hypothesis that ACE is a possible candidate gene for primary hypertension in humans. We defined the genotypes and allele frequencies of an insertion-deletion (I/D) polymorphism in parental couples who both had either high or low blood pressure and in their offspring.

Subjects: Parents (n = 111) and offspring (n = 75) with defined blood pressure status from the Dutch Hypertension and Offspring Study.

Methods: Genomic DNA was amplified by polymerase chain reaction using primers flanking the polymorphic region in intron 16 of the ACE gene. Alleles were detected on agarose gels stained with ethidium bromide.

Results: Allele frequencies for the D-allele were similar in parents with high (0.66) and low blood pressure (0.59) and in their offspring (0.67 and 0.69, respectively). A similar lack of difference was found with respect to the complementary I-allele.

Conclusions: In the present rather large sample we failed to find a significant association between I/D polymorphism of the ACE gene and blood pressure status in subjects with high or low blood pressure and in their offspring.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Alleles
  • Base Sequence
  • DNA / genetics
  • Female
  • Gene Frequency
  • Genetic Markers
  • Genotype
  • Humans
  • Hypertension / enzymology*
  • Hypertension / epidemiology
  • Hypertension / genetics*
  • Male
  • Middle Aged
  • Molecular Sequence Data
  • Netherlands / epidemiology
  • Peptidyl-Dipeptidase A / genetics*
  • Polymorphism, Genetic*
  • Repetitive Sequences, Nucleic Acid
  • Sequence Deletion


  • Genetic Markers
  • DNA
  • Peptidyl-Dipeptidase A