Why the study?
Essential hypertension is a complex disorder involving genetic and non-genetic factors, prompting investigation into the association of RAAS gene SNPs with essential hypertension in a North-Indian population.
Are ACE, AGT, and REN nucleotide variants associated with essential hypertension in the North Indian population?
Are ACE, AGT, and REN nucleotide variants associated with essential hypertension in the North Indian population?
Specific SNPs in the AGT and REN genes are associated with an increased risk of essential hypertension, while an ACE variant is associated with decreased risk in a North Indian population.
Introduction Essential hypertension (EH) is a chronic condition characterized by elevated blood pressure without any identifiable cause. Being a complex disorder, EH involves both genetic and non-genetic factors. This study investigated the association of RAAS genes- AGT, ACE , and REN SNPs with EH in the North-Indian population of Jammu. Methodology A total of 805 participants (392-cases; 413-controls) were genotyped for seven SNPs. Logistical regression, t-test, and Chi-square statistics were used to calculate the significance levels. Results Out of the seven SNPs, AGT /rs1926722 and REN /rs2368564 showed a significant positive correlation with EH [OR = 1.58 (95% CI:1.02–2.45, adj. P = 0.03) and OR = 1.45 (95% CI:1.08–1.94, adj. P = 0.01), respectively]. The ACE /rs4295, on the contrary, showed a significant negative correlation with EH [OR = 0.67 (95% CI:0.49–0.90), adj. P = 0.008]. Interestingly, these correlations were found to be restricted to systolic pressure. The gene-gene interaction analysis revealed an additive interaction between AGT /rs1926722 and REN /rs2368564 and an antagonistic interaction between ACE /rs4295 and AGT /rs1926722 or REN /rs2368564. Conclusion The positive correlation of AGT /rs1926722 and REN /rs2368564 suggests an increased risk for EH, whereas the negative correlation of ACE /rs4295 with EH suggests a decreased risk for EH in the study population. To better understand the genetic causes of EH in the study population, it is necessary to screen more variants in the RAAS and other blood pressure-related genes.
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Kavinay et al. (2025) studied this question.
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