48 Polymorphisms In α‐Adducin (G460w) and G‐Protein β‐3 Subunit (C825t) Genes In Essential Hypertension

Abstract

Objectives Essential hypertension (EH) has a multifactorial origin and is thought to arise from an interaction between susceptibility genes and environmental factors. A number of candidate genes have been proposed. In our study, the role of polymorphisms in α‐adducin (ADD1) and G‐protein β‐3 subunit (GNB3) genes in EH was investigated.Design and Methods Ninety‐three children and young adults, aged from 4 to 27 years, with both parents, were included in our study, giving 93 nuclear families. Two polymorphisms were detected using the polymerase chain reaction technique (PCR). Investigating the C825T polymorphism of GNB3 the C allele was identified by the presence of 152 and 116 bp signals and the T allele was present when a non‐digested 268 bp long band was detected. The allele‐specific polymerase chain reaction (PCR) was used to study the G460W polymorphism of ADD1. For statistical analysis the transmission disequilibrium test (TDT) was used. By using non‐transmitted alleles as the control population, problems of population admixture and mismatched controls are avoided.Results The following genotype frequencies for G460W polymorphism in ADD1gene were observed: 67 (72.0%) were GG homozygotes, 23 (24.7%) were GW heterozygotes and 3 (3.3%) were WW homozygotes. Using the TDT test, 44 nuclear families were used. There were 63 transmitted G alleles, 25 transmitted W alleles, 60 non‐transmitted G alleles and 28 non‐transmitted W alleles. The observed difference was not statistically significant (χ2 = 0.24, P = 0.62).The following genotype frequencies for the C825T polymorphism in GNB3 gene were found: 50 (53.8%) were CC homozygotes, 35 (37.6%) were CT heterozygotes and 8 (8.6%) were TT homozygotes. 73 nuclear families were used. There were 95 transmitted C alleles, 51 transmitted T alleles, 84 non‐transmitted C alleles and 62 non‐transmitted T alleles. The observed difference again was not statistically significant (χ2 = 1.75, P = 0.19).Conclusions Our study found no association of the polymorphisms in ADD1 and GNB3 genes with EH, respectively. However, our sample size was rather small. It seems very likely that many genes with small effects (such as the gene variants above) account for the heritability of EH.