title: Repeated blood pressure measurements in a sample of Swedish twins: heritabilities and associations with polymorphisms in the renin-angiotensin-aldosterone system.
abstract: BACKGROUND
  Twin and family studies have shown that genetic effects explain a relatively high amount of the phenotypic variation in blood pressure. However, many studies have not been able to replicate findings of association between specific polymorphisms and diastolic and systolic blood pressure.
  
  
  METHODS
  In a structural equation-modelling framework the authors investigated longitudinal changes in repeated measures of blood pressures in a sample of 298 like-sexed twin pairs from the population-based Swedish Twin Registry. Also examined was the association between blood pressure and polymorphisms in the angiotensin-I converting enzyme and the angiotensin II receptor type 1 with the 'Fulker' test. Both linkage and association were tested simultaneously revealing whether the polymorphism is a Quantitative Trait Locus (QTL) or in linkage disequilibrium with the QTL.
  
  
  RESULTS
  Genetic influences explained up to 46% of the phenotypic variance in diastolic and 63% of the phenotypic variance in systolic blood pressure. Genetic influences were stable over time and contributed up to 78% of the phenotypic correlation in both diastolic and systolic blood pressure. Non-shared environmental effects were characterised by time specific influences and little transmission from one time point to the next. There was no significant linkage and association between the polymorphisms and blood pressure.
  
  
  CONCLUSIONS
  There is a considerable genetic stability in both diastolic and systolic blood pressure for a 6-year period of time in adult life. Non-shared environmental influences have a small long-term effect. Although associations with the polymorphisms could not be replicated, results should be interpreted with caution due to power considerations.
authors.affiliation: Department of Medical Epidemiology, Karolinska Institutet, Stockholm, Sweden. anastasia.iliadou@mep.ki.se
authors.forename: Anastasia
authors.initials: A
authors.lastname: Iliadou
authors.forename: Paul
authors.initials: P
authors.lastname: Lichtenstein
authors.forename: Ralf
authors.initials: R
authors.lastname: Morgenstern
authors.forename: Lena
authors.initials: L
authors.lastname: Forsberg
authors.forename: Richard
authors.initials: R
authors.lastname: Svensson
authors.forename: Ulf
authors.initials: U
authors.lastname: de Faire
authors.forename: Nicholas G
authors.initials: NG
authors.lastname: Martin
authors.forename: Nancy L
authors.initials: NL
authors.lastname: Pedersen
mesh_terms: D000368:Aged; D001794:Blood Pressure / Q000235:genetics*; D005260:Female; D006801:Humans; D015810:Linkage Disequilibrium; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics; D010641:Phenotype; D011110:Polymorphism, Genetic; D040641:Quantitative Trait Loci; D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin / Q000235:genetics; D012084:Renin-Angiotensin System / Q000235:genetics*; D013548:Sweden; D014429:Twins, Dizygotic / Q000235:genetics*; D014430:Twins, Monozygotic / Q000235:genetics*
chemical_list: D044140:Receptor, Angiotensin, Type 1; D011945:Receptors, Angiotensin; D007703:Peptidyl-Dipeptidase A