A gene designated S-A has been implicated in hypertension (HT) in rat
genetic models and Japanese HT patients. However, a linkage study in w
hites was negative. Because of the limitations of genetic analyses, co
nfirmation in different settings is imperative. Therefore, we conducte
d a cross-sectional case-control study involving 106 HT and 96 normote
nsive (NT) white subjects. A polymerase chain reaction technique was d
eveloped for PstI restriction fragment length polymorphism (RFLP) dete
rmination. We could find no association of this RFLP with HT (frequenc
y of minor allele, A2 = 0.11 in HTs v 0.07 in NTs). However, A2 displa
yed an association with increase in body mass index in HTs: for a body
mass index mean of 26 kg/m(2) or more, A2 = 0.17 compared to 0.06 for
body mass index of less than 26 kg/m(2) (chi(2) = 6.4, P = .01; odd r
atio 3.4, 95% confidence interval 1.2 to 10.0); for a body mass index
of 28 kg/m(2) or more, A2 = 0.20 (chi(2) = 10.4, P = .001; odds ratio
4.0, 95% confidence interval 1.5 to 10.5). Furthermore, A2 tracked sig
nificantly with elevation in body mass index in the HTs (F = 4.8, P =
.01 by one-way ANOVA). In conclusion, we could find no association of
S-A genotype with HT, but obtained preliminary evidence for a possible
association with variation in body mass index in a severely affected
HT group with a strong family history of HT. (C) 1997 American Journal
of Hypertension, Ltd.