title: Angiotensin II type 1 receptor gene A1166C polymorphism is associated with the increased risk of pregnancy-induced hypertension.
abstract: OBJECTIVE
  The aim of our study was to evaluate the relation of parental history of hypertension to the development of PIH, and to assess the potential role of plausible candidate loci in the susceptibility to PIH.
  
  
  METHODS
  Five polymorphisms: ACE gene I/D and Pst1 RFLP polymorphism, AGT gene M235T polymorphism, AGTR1 gene A1166C polymorphism, and chymase gene CMA/B polymorphism were studied in 126 women suffering from PIH in comparison with 150 healthy pregnant women. Genotyping was performed using methods based on polymerase chain reaction.
  
  
  RESULTS
  Among the PIH patients, positive parental history of hypertension (hypertension in both parents, in mother alone or in father alone) was significantly more frequent than in healthy pregnant women. Having a hypertensive father or mother statistically significantly increased the risk of PIH (odds ratio 4.34, 95% CI, 1.86-10.13, and 2.33, 95% CI, 1.29-4.12 respectively). CC genotype was significantly more frequent in women with PIH as compared with healthy controls and the C allele frequency was also significantly higher among the cases compared to controls. Having a CC genotype increased the risk of development of PIH 2.74 times (95% CI, 1.08-6.97). We observed no significant differences in genotype distributions or the allele frequencies of other examined polymorphisms.
  
  
  CONCLUSIONS
  On the basis of the results of our study, we may suggest that AGTR1 gene A1166C polymorphism may predispose women to the development of PIH. It seems that ACE gene I/D and Pst1 RFLP polymorphism, AGT gene M235T polymorphism, and finally chymase gene CMA/B polymorphism do not play any significant role in the pathogenesis of PIH in Caucasian women.
authors.affiliation: Department and Clinic of Internal Medicine and Diabetology, Silesian Medical University, ul. 3. Maja 13/15, 41-800 Zabrze, Poland. kchwdlab@medyk1.slam.katowice.pl
authors.forename: K
authors.initials: K
authors.lastname: Nałogowska-Głośnicka
authors.forename: B I
authors.initials: BI
authors.lastname: Łacka
authors.forename: M J
authors.initials: MJ
authors.lastname: Zychma
authors.forename: W
authors.initials: W
authors.lastname: Grzeszczak
authors.forename: E
authors.initials: E
authors.lastname: Zukowska-Szczechowska
authors.forename: R
authors.initials: R
authors.lastname: Poreba
authors.forename: B
authors.initials: B
authors.lastname: Michalski
authors.forename: B
authors.initials: B
authors.lastname: Kniazewski
authors.forename: J
authors.initials: J
authors.lastname: Rzempołuch
mesh_terms: D000293:Adolescent; D000328:Adult; D053818:Chymases; D004247:DNA / Q000097:blood; D015252:Deoxyribonucleases, Type II Site-Specific; D005260:Female; D020022:Genetic Predisposition to Disease; D018392:Genomic Imprinting; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000453:epidemiology / Q000235:genetics*; D008297:Male; D009679:Nuclear Family; D011044:Poland; D011110:Polymorphism, Genetic; D012150:Polymorphism, Restriction Fragment Length; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000453:epidemiology*; D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin / Q000235:genetics*; D012016:Reference Values; D012307:Risk Factors; D012697:Serine Endopeptidases / Q000235:genetics; D044465:White People
chemical_list: D044140:Receptor, Angiotensin, Type 1; D044139:Receptor, Angiotensin, Type 2; D011945:Receptors, Angiotensin; D004247:DNA; C024388:CTGCAG-specific type II deoxyribonucleases; D015252:Deoxyribonucleases, Type II Site-Specific; D012697:Serine Endopeptidases; D053818:Chymases