title: Familial and phenotypic associations of the aldosterone Renin ratio.
abstract: BACKGROUND
  The aldosterone to renin ratio (ARR) is a marker of aldosterone excess, widely used to screen for primary aldosteronism (PA). The significance of a raised ARR in normotensive and hypertensive subjects and the phenotypic and familial factors affecting it are unclear.
  
  
  OBJECTIVE
  We estimated the distribution and heritability of the ARR and tested for associations between ARR and blood pressure (BP) with 11 polymorphisms at the CYP11B1/CYP11B2 locus.
  
  
  METHODS
  A total of 1172 individuals from 248 Caucasian families ascertained via a hypertensive proband were evaluated.
  
  
  METHODS
  Plasma aldosterone was measured by RIA, and plasma renin concentration was measured by the LIAISON Direct Renin chemiluminescent immunoassay.
  
  
  RESULTS
  Unadjusted and adjusted ARR were continuously distributed in normotensives and hypertensives, with no evidence of a cutoff that would identify a separate population with PA. Median ARR was 4.19 ng/liter per mIU/liter (range, 0.04-253.16). ARR levels were higher in females and associated with age, body mass index, and potassium. Antihypertensive agents had significant predictable effects on the ARR. Renin was negatively associated, and ARR was positively associated with ambulatory BP readings (P < 0.001) in subjects not taking antihypertensives. The heritability of the ARR was 38.1% (P < 10(-8)). Plasma aldosterone, but not ARR, was influenced by the intron 2 conversion variation in the CYP11B2 gene (beta = -0.07; P = 0.04).
  
  
  CONCLUSIONS
  The ARR is continuously distributed, is influenced by genetic and environmental factors, and is not a marker of a distinct pathological abnormality but possibly reflects the long-term influence of aldosterone on cardiovascular homeostasis.
authors.affiliation: Faculty of Medicine, University of Glasgow, British Heart Foundation Glasgow Cardiovascular Research Centre, Glasgow G12 8TA, United Kingdom.
authors.forename: Samantha
authors.initials: S
authors.lastname: Alvarez-Madrazo
authors.forename: Sandosh
authors.initials: S
authors.lastname: Padmanabhan
authors.forename: Bongani M
authors.initials: BM
authors.lastname: Mayosi
authors.forename: Hugh
authors.initials: H
authors.lastname: Watkins
authors.forename: Peter
authors.initials: P
authors.lastname: Avery
authors.forename: A Michael
authors.initials: AM
authors.lastname: Wallace
authors.forename: Robert
authors.initials: R
authors.lastname: Fraser
authors.forename: Eleanor
authors.initials: E
authors.lastname: Davies
authors.forename: Bernard
authors.initials: B
authors.lastname: Keavney
authors.forename: John M
authors.initials: JM
authors.lastname: Connell
mesh_terms: D000328:Adult; D000450:Aldosterone / Q000097:blood / Q000235:genetics*; D001794:Blood Pressure / Q000502:physiology; D015992:Body Mass Index; D002940:Circadian Rhythm; D005190:Family; D005260:Female; D005838:Genotype; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000235:genetics* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D010641:Phenotype; D012083:Renin / Q000097:blood / Q000235:genetics*; D044465:White People
chemical_list: D000450:Aldosterone; D012083:Renin