Zheng Liu, Jingjing Wu, Jie Zhang, Yezhou Liu, Bin Liu, Jiapeng Lu, Yuxiang Yan and Ling Zhang
Background: PRKG1 plays an important role in regulating vascular smooth muscle contraction. And this gene is regarded as one of the candidate genes on salt-sensitive hypertension. The aim of this study was to investigate the effects of environmental risk factors and two SNPs and haplotypes structures of PRKG1 gene with blood salt-sensitive patients among essential hypertension.
Method: Three hundred and forty-two essential hypertensive were recruited in a case-case study, a modified Sullivan’s acute salt load method was conducted to identify the salt-sensitivity and salt-resistant. Medical history and lifestyle risk factors were obtained by questionnaire, and blood and urine specimens were collected to test the biochemical indicators. We used the Sequenom Mass ARRAY Platform for genotyping of PRKG1 gene single nucleotide polymorphisms (SNPs) (rs7897633/SNP1, rs1904694/SNP2). We applied statistical software SPSS17.0, multifactor dimensionality reduction method 1.1.0 and haploview 4.0 to do the analyses.
Results: There were 63 salt sensitivity subjects in 342 essential hypertension individuals, accounting for 18.4% of the total. Age and 24-hour urinary sodium concentration were the risk factors associated with salt-sensitive hypertension. The results of the logistic regression model showed that subjects carrying SNP1-AA genotype and SNP2-GG genotypes had 2.83-fold (95% CI: 1.21-6.63) and 3.50-fold (95% CI: 1.54-7.93) risks to have salt-sensitive hypertension, respectively. Haplotype analysis showed that haplotype CA had 0.56-fold (95% CI: 0.38-0.84) decreased risk for salt-sensitive hypertension, whereas, haplotype AG had 1.78-fold (95% CI: 1.20-2.65) increased risk for saltsensitive hypertension.
Conclusion: Age and 24-hour urinary sodium concentration are the environmental risk factors associated with salt-sensitive hypertension. Genotypes of SNP1-AA, SNP2-GG and haplotype AG of PRKG1 gene were risk factors for salt-sensitivity in essential hypertension.
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