title: SAH gene variants revisited in the European Project On Genes in Hypertension.
abstract: OBJECTIVE
  Previous studies found significant association of hypertension and hypertension-related phenotypes with genetic variation in SAH (Spontaneously hypertensive rat-clone A-Hypertension-associated). We sought independent confirmation of these findings in the European Project On Genes in Hypertension.
  
  
  RESULTS
  We randomly recruited 2603 relatives from 560 families and 31 unrelated subjects from six European populations (mean age 38.8 +/- 15.7 years; 52.1% women). We measured systolic/diastolic blood pressure (mean, 122.4/76.6 mmHg), body mass index (24.9 kg/m2), triceps skinfold (1.7 cm), waist-to-hip ratio (0.83 units), serum total and high-density lipoprotein (HDL) cholesterol (5.14 and 1.33 mmol/l), serum triglycerides (1.95 mmol/l) and blood glucose (4.90 mmol/l). We genotyped the G-1606A and -962del/ins polymorphisms. In all subjects, the allele frequencies were 11.8 and 29.5% for -1606A and -962del, respectively. Lewontin's D' was 0.97 (P < 0.0001). Haplotype frequencies were 58.8% for -1606G plus -962ins, 29.5% for -1606G plus -962del, and 11.7% for -1606A plus -962ins. Both before and after adjustment for covariates, none of the phenotype-genotype associations approached statistical significance. Our study had 80% power to detect on two-sided tests (P = 0.05), effect sizes of 1.8/1.3 mmHg for systolic/diastolic blood pressure, 0.52 kg/m2 for body mass index, 0.01 units for the waist-to-hip ratio, 0.96 mm for the triceps skinfold, 0.13 and 0.05 mmol/l for total and HDL cholesterol, 0.18 mmol/l for serum triglycerides, and 0.11 mmol/l for blood glucose. The family-based analyses did not reveal population stratification (P > or = 0.67).
  
  
  CONCLUSIONS
  The evidence supporting an association of hypertension or hypertension-related phenotypes with the SAH gene remains equivocal in human studies.
authors.affiliation: Department of Clinical and Experimental Medicine, University of Padova, Italy.
authors.forename: Valérie
authors.initials: V
authors.lastname: Tikhonoff
authors.forename: Jan A
authors.initials: JA
authors.lastname: Staessen
authors.forename: Tatiana
authors.initials: T
authors.lastname: Kuznetsova
authors.forename: Lutgarde
authors.initials: L
authors.lastname: Thijs
authors.forename: Sandra
authors.initials: S
authors.lastname: Hasenkamp
authors.forename: Veronika
authors.initials: V
authors.lastname: Bäumer
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Stolarz
authors.forename: Jitka
authors.initials: J
authors.lastname: Seidlerová
authors.forename: Jan
authors.initials: J
authors.lastname: Filipovský
authors.forename: Yuri
authors.initials: Y
authors.lastname: Nikitin
authors.forename: Jan
authors.initials: J
authors.lastname: Peleska
authors.forename: Kalina
authors.initials: K
authors.lastname: Kawecka-Jaszcz
authors.forename: Edoardo
authors.initials: E
authors.lastname: Casiglia
authors.forename: Stefan-Martin
authors.initials: SM
authors.lastname: Brand-Herrmann
authors.forename: Eva
authors.initials: E
authors.lastname: Brand
mesh_terms: D000328:Adult; D001786:Blood Glucose; D001794:Blood Pressure / Q000235:genetics*; D015992:Body Mass Index; D003066:Coenzyme A Ligases / Q000235:genetics*; D015331:Cohort Studies; D005260:Female; D006239:Haplotypes; D006801:Humans; D006973:Hypertension / Q000235:genetics*; D008074:Lipoproteins / Q000097:blood; D008297:Male; D008875:Middle Aged; D020641:Polymorphism, Single Nucleotide / Q000235:genetics*; D044465:White People
chemical_list: D001786:Blood Glucose; D008074:Lipoproteins; C487181:ACSM3 protein, human; D003066:Coenzyme A Ligases