Polymorphism of α-adducin and hypertension

Vol 350 • August 2, 1997 369 (sense) and 5'-CTGCAGCAAGGGTTTCACGTGATTG-3' (antisense), according to the previously published sequence. The genotype was determined by allele-specific oligonucleotide hybridisation, and we confirmed the validity of the method by direct sequencing in several samples. The frequencies of the 460Trp allele in our study population (0·529 in normotensives and 0·656 in hypertensives) were much higher than those reported in European populations (0·136–0·238). The frequency of the genotype of the Gly460Trp polymorphism differed significantly between hypertensive and normotensive groups (p=0·0087). A multiple logistic analysis with sex, age, body-mass index, and the genotype of the -adducin gene (Gly/Gly=0, Gly/Trp+Trp/Trp=1) as independent variables, and blood pressure status (normotensive or hypertensive) as the dependent variable showed that bodymass index (p=0·0009) and the genotype of the -adducin gene (p=0·0124) were predictors of bloodpressure status (p<0·0001). The odds ratio for hypertension associated with the presence of one or two 460Trp alleles, compared with a person homozygous for the 460Gly allele, was 2·82 (95% CI 6·37–1·25). The 460Trp allele was significantly associated with lower plasma renin activity in a subgroup of hypertensives in whom renin activity was assessed in the outpatient clinic after 30 min of rest (n=55). On the other hand, this polymorphism had no significant effects on left-ventricular mass corrected by height as assessed by echocardiography (n=90). Our findings suggest that the Trp460Gly polymorphism of the -adducin gene seems to be involved in hypertension, possibly of the lowrenin type, among Japanese.