Essential arterial hypertension and polymorphism of angiotensinogen M235T gene

J Cell Mol Med. 2002 Apr-Jun;6(2):245-50. doi: 10.1111/j.1582-4934.2002.tb00191.x.

Abstract

Several candidate genes, chosen from the renin- angiotensin system, were examined for their association with essential hypertension. The genes of the renin- angiotensin system (RAS) are good candidates for such an approach because this system is well known to be involved in the control of blood pressure. One of these candidate genes is the gene encoding for angiotensinogen (the most important gene of the RAS associated with essential hypertension in the most population, is the gene for angiotensin-converting enzyme- ACE). One DNA polymorphism within exon 2- with threonine instead of methionine at position 235 (M235T) was found to be significantly associated with hypertension. The objective of this study is the analysis of M235T polymorphism in angiotensinogen gene in Romanian patients with essential hypertension as well as controls. We examined 38 patients with essential hypertension and 21 normotensive patients. In order to identify the M235T angioteninogen variant, we used the following methods: DNA extraction, PCR amplification and enzymatic digestion of the PCR product using Tth 111I restriction endonuclease enzyme. In the study groups, the M235T variant (Met?Thr in aminoacid position 235) was found more frequently in hypertensive patients (81,57%), than in control subjects (66,66%). We identified 52,63% M235T heterozygotes in the hypertensive group compared with 47,61% in the control group, and 28,94% T235T homozygotes in the hypertensive group compared with 19,04% in the control group. The results of our study suggest an association of the M235T polymorphism in the gene encoding angiotensinogen with essential hypertension.

Publication types

  • Comparative Study

MeSH terms

  • Adult
  • Aged
  • Amino Acid Substitution
  • Angiotensinogen / genetics*
  • Gene Frequency
  • Genotype
  • Humans
  • Hypertension / genetics*
  • Male
  • Middle Aged
  • Peptidyl-Dipeptidase A / genetics
  • Point Mutation
  • Polymorphism, Genetic*

Substances

  • Angiotensinogen
  • Peptidyl-Dipeptidase A