title: Interaction between the angiotensin-converting enzyme gene insertion/deletion polymorphism and obstructive sleep apnoea as a mechanism for hypertension.
abstract: OBJECTIVE
  Obstructive sleep apnoea (OSA) confers a risk of hypertension and cardiovascular complications. Both the renin-angiotensin-aldosterone system and OSA are important determinants of blood pressure, but it is not fully known how they interact. The aim of this study was to explore the interaction between the angiotensin-converting enzyme (ACE) gene insertion/deletion (I/D) polymorphism and OSA in the association with hypertension.
  
  
  METHODS
  A community-based, case-control design with hypertensive patients in primary care (n = 157) and normotensive population controls (n = 181).
  
  
  METHODS
  All subjects underwent ambulatory polysomnography during one night. OSA was defined by a minimum of 10 apnoea/hypopnoea events per hour. Office blood pressure was measured and hypertension status was assessed. The genotypes were determined using polymerase chain reaction.
  
  
  RESULTS
  An interaction analysis including sex, ACE I/D polymorphism (DD and ID versus II), and OSA identified a significant interaction between OSA and the ACE I/D polymorphism: odds ratio (OR) 6.3, 95% confidence interval (CI) 1.8-22.5, P = 0.004 as well as between OSA and sex: OR 3.3, 95% CI 1.1-9.6, P = 0.033. OSA was significantly associated with hypertension in men but not in women.
  
  
  CONCLUSIONS
  The interaction between the ACE gene I/D polymorphism and OSA appears to be an important mechanism in the development of hypertension, particularly in men.
authors.affiliation: Department of Clinical Sciences, Diabetes and Endocrinology, Skaraborg Institute, Skövde, Sweden. kristina.a.bengtsson@vgregion.se
authors.forename: Kristina Bengtsson
authors.initials: KB
authors.lastname: Boström
authors.forename: Jan
authors.initials: J
authors.lastname: Hedner
authors.forename: Olle
authors.initials: O
authors.lastname: Melander
authors.forename: Ludger
authors.initials: L
authors.lastname: Grote
authors.forename: Bo
authors.initials: B
authors.lastname: Gullberg
authors.forename: Lennart
authors.initials: L
authors.lastname: Råstam
authors.forename: Leif
authors.initials: L
authors.lastname: Groop
authors.forename: Ulf
authors.initials: U
authors.lastname: Lindblad
mesh_terms: D000328:Adult; D000483:Alleles; D001794:Blood Pressure / Q000235:genetics; D016022:Case-Control Studies; D005260:Female; D017353:Gene Deletion; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease / Q000235:genetics; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000235:genetics*; D016015:Logistic Models; D008297:Male; D008875:Middle Aged; D007703:Peptidyl-Dipeptidase A / Q000235:genetics*; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic; D017286:Polysomnography; D012107:Research Design; D012737:Sex Factors; D020181:Sleep Apnea, Obstructive / Q000150:complications / Q000235:genetics*; D013548:Sweden
chemical_list: D007703:Peptidyl-Dipeptidase A