Essential arterial hypertension and polymorphism of angiotensiongen M235T gene

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 IIII 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

Glucocorticoid exposure in late gestation in the rat permanently programs gender-specific differences in adult cardiovascular and metabolic physiology

“…Similarly, mutations in the angiotensinogen gene are associated with hypertension in humans (18,41,53). It has been suggested that angiotensinogen is not merely a passive substrate reservoir but also stabilizes plasma renin concentrations (by decreasing its metabolic clearance) (15).…”

Estimation of risk and interaction of single nucleotide polymorphisms at angiotensinogen locus causing susceptibility to essential hypertension: a case control study

“…PCR reactions and genotyping of -217G>A, -152G>A, -6G>A, T174M and M235T variants were done as described in detail elsewhere. 2,37,38,39 For -20A>C primers were designed (sense: 5' GCT TCT GGC ATC TGT CCT TC 3' and antisense: 5' CCG GCT TAC CTT CTG CTG TA 3') and genotyping was done by digesting 5 µl of the PCR product (protocol and conditions for PCR was similar to those used for the above mentioned polymorphisms except for the annealing temperature, which was 60°C for 50 sec) with 1.5 units of EcoO109 I restriction enzyme followed by electrophoresis using 3.5% agarose gel. The genotypes were identified based on the presence of bands representing allele A (AA -187 bp) or allele C (CC -124 bp and 63 bp) or both (AC -187 bp, 124 bp and 63 bp).…”

Association of Т174М polymorphism of the angiotensinogen gene with the higher risk of cerebral stroke in women

“…Ген AGT локализован на длинном плече 1-й хромосо-мы в локусе 1q42-q43, содержит 5 экзонов молекулярной массой 62-65 кДа [18]. В результате действия ренина от ангиотензиногена (АГТ) отщепляется концевой декапеп-тид, который и представляет собой ангиотензин I. Он пре-образуется в ангиотензин II (АТII) под действием ангио-тензинпревращающего фермента (АПФ).…”