In Milan hypertensive rats, a variant in the alpha-adducin gene has been sh
own to account for approximately 50% of the interindividual variation in bl
ood pressure levels between these animals and their normotensive counterpar
ts. Additional studies have suggested that a polymorphism within exon 10 of
the human alpha-adducin gene (Gly-460-Trp) may be associated with hyperten
sion and salt sensitivity. On the basis of these observations, we investiga
ted variation within or near the human cu-adducin gene for linkage and asso
ciation with a locus influencing blood pressure levels in 281 nuclear famil
ies (774 siblings aged 5 to 37 years; 380 parents aged 26 to 57 years), sel
ected from the white population of Rochester, Minnesota, without regard to
health. Sib pair linkage analyses (n = 852 sibling pairs) using a dinucleot
ide repeat marker (D4S43) that maps approximately 660 kb from the alpha-add
ucin gene provided no evidence of linkage between this marker locus and a l
ocus influencing systolic, diastolic, or mean blood pressure levels. Allele
frequencies for the Gly-460-Trp polymorphism were similar to those reporte
d in other white populations (Gly = 0.812, Trp = 0.188); however, this poly
morphism was not associated with any measure of blood pressure level in eit
her parents or siblings. Therefore, variation within the alpha-adducin gene
does not appear to have a major influence on measures of blood pressure in
white families from Rochester, Minnesota. Am J Hypertens 2000;13:699-703 (
C) 2000 American Journal of Hypertension, Ltd.