Effect of the rs198389 polymorphism of the NPPB gene on ambulatory blood pressure monitoring parameters in uzbek hypertensive patients
F T Saidakbarova, R B Aliyeva, N Z SrojidinovaAbstract
Objective
To assess ambulatory blood pressure monitoring (ABPM) parameters according to the rs198389 polymorphism of the NPPB gene in hypertensive patients with and without type 2 diabetes mellitus (T2DM).
Materials and Methods
The study included 196 Uzbek hypertensive patients, of whom 100 had T2DM and 96 didn't have DM. ABPM was performed using a Medicom-Combi device by the oscillometric method. Genomic DNA was extracted using the Vazyme Fast Pure Blood DNA Isolation Mini Kit-BOX2 (China). The rs198389 polymorphism of the NPPB gene was genotyped using real-time PCR. Statistical analyses were conducted using IBM SPSS Statistics for Windows, version 27.
Results
In patients with HNT and T2DM, carriers of the AA genotype demonstrated significantly higher mean daytime SBP and DBP compared with AG and GG genotype carriers (mean daytime SBP: 152.12±7.5 vs 148.5±7.8 vs 143.4±8.6 mmHg, p=0.03; mean daytime DBP: 88.5±9.3 vs 81.2±9.1 vs 81.9±9.6 mmHg, p=0.023). Nighttime SBP variability was also higher in AA genotype carriers (14.2±4.8 vs 12.2±3.7 vs 12.8±3.6 mmHg, p=0.054). In the non-diabetic group, the mean daytime SBP was significantly higher in patients with the AA genotype than in those with the AG and GG genotypes (138.5±15.8 vs 130.7±14.4 vs 128.2±12.6 mmHg, p=0.04). Daytime SBP variability was also significantly higher in AA genotype carriers (15.3±7.1 vs 14.3±5.8 vs 12.0±4.0 mmHg, p=0.05). Allele-based analysis revealed a consistent tendency toward higher ABPM parameters in A-allele carriers. In patients with HNT and T2DM, mean 24-hour and daytime SBP, as well as mean nighttime SBP and DBP, were significantly higher in A-allele carriers than in G-allele carriers (mean 24-hour SBP: 154.02±6.5 vs 148.08±6.8 mmHg, p=0.045; mean daytime SBP: 151.7±7.6 vs 145.4±8.1 mmHg, p=0.04). Nighttime SBP variability was also significantly higher in A-allele carriers (13.5±4.6 vs 12.2±3.0 mmHg, p=0.05). In the non-diabetic group, the mean 24-hour SBP was significantly higher in A-allele carriers (135.4±15.7 vs 128.9±14.8 mmHg, p=0.05). Higher nighttime BP values were also observed in A-allele carriers (mean nighttime SBP: 126.9±33.2 vs 117.9±28.1 mmHg, p=0.048; mean nighttime DBP: 76.2±20.1 vs 65.2±17.3 mmHg, p=0.052). Evaluation of BP variability demonstrated significantly higher daytime and nighttime SBP and DBP variability indices in the A-allele carriers than in the G-allele carriers (daytime SBP variability: 15.2±6.6 vs 11.2±5.1 mmHg (p=0.054); daytime DBP variability: 14.4±4.4 vs 12.1±4.9 mmHg (p=0.05); nighttime SBP variability: 12.4±4.3 vs 10.2±5.4 mmHg (p=0.05); nighttime DBP variability: 11.5±4.2 vs 10.0±4.7 mmHg, p=0.02).
Conclusion
The AA genotype and the A allele of the rs198389 polymorphism of the NPPB gene were associated with higher BP levels and greater variability, indicating a potential role of this genetic variant in the regulation of the BP circadian patterns in the Uzbek population.