Abstract
A gene designated S(A) has been implicated in hypertension (HT) in rat genetic models and Japanese HT patients. However, a linkage study in whites was negative. Because of the limitations of genetic analyses, confirmation in different settings is imperative. Therefore, we conducted a cross-sectional case-control study involving 106 HT and 96 normotensive (NT) white subjects. A polymerase chain reaction technique was developed for PstI restriction fragment length polymorphism (RFLP) determination. We could find no association of this RFLP with HT (frequency of minor allele, A2 = 0.11 in HTs v 0.07 in NTs). However, A2 displayed an association with increase in body mass index in HTs: for a body mass index mean of 26 kg/m2 or more, A2 = 0.17 compared to 0.06 for body mass index of less than 26 kg/m2 (chi2 = 6.4, P = .01; odd ratio 3.4, 95% confidence interval 1.2 to 10.0); for a body mass index of 28 kg/m2 or more, A2 = 0.20 (chi2 = 10.4, P = .001; odds ratio 4.0, 95% confidence interval 1.5 to 10.5). Furthermore, A2 tracked significantly 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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have