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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Sodium and potassium intake represent major modifiable environmental factors influencing blood pressure (BP). Urinary sodium-to-potassium (Na/K) ratio strongly associates with elevated BP, but whether genetic and environmental factors modify this association remains unclear. Furthermore, the interplay between genetic predisposition, aging, and body mass index (BMI) on BP regulation has not been fully elucidated. We examined how genetic and environmental factors modify the association between urinary Na/K ratio and BP. Additionally, we explored how genetic predisposition to hypertension interacts with age, BMI, and sex in determining systolic BP (sBP), diastolic BP (dBP), and pulse pressure (PP).
From UK Biobank (UKB) participants aged 40-69 years, we selected individuals not taking antihypertensives who had complete data on BP, urinary Na/K ratio, polygenic risk score (PRS) for incident hypertension (available in UKB), lifestyle habits, and laboratory parameters. We constructed multiple linear regression models with sBP, dBP, and PP as outcomes. Independent variables included urinary Na/K ratio, PRS, age, sex, BMI, and relevant covariates. To examine gene-environment and gene-lifestyle interactions, we analyzed interaction terms between urinary Na/K ratio and age, BMI, and PRS, and between PRS and age, BMI.
Among 303,993 individuals (mean age 55.4 ± 8.1 years, 43.4% male), both urinary Na/K ratio and PRS were significantly associated with all BP parameters (P < 0.001). Per 1-SD increase in standardized variables, urinary Na/K ratio showed associations with sBP (β = 2.32), dBP (β = 0.79), and PP (β = 1.53), while PRS showed associations with sBP (β = 3.17), dBP (β = 1.69), and PP (β = 1.48). Interaction analyses revealed that the effect of urinary Na/K ratio on BP was amplified with older age (interaction β = 0.50, 0.15, and 0.48 for sBP, dBP, and PP, respectively; P < 0.001 for all) and attenuated at higher BMI levels (interaction β = -0.33, -0.18, and -0.23; P < 0.001 for all). PRS showed a significant positive interaction with Na/K ratio only for dBP (β = 0.05, P = 0.009).
Age-PRS interaction analyses demonstrated contrasting patterns: for sBP, a positive interaction (β = 0.25, P < 0.001) indicated amplification of genetic effects with aging, while for dBP, a negative interaction (β = -0.085, P < 0.001) suggested attenuation. For PP, a strong positive interaction (β = 0.36, P < 0.001) was observed, indicating marked genetic amplification with age, likely reflecting arterial stiffening. In contrast, BMI showed negative interactions with PRS for both sBP (β = -0.116, P < 0.001) and dBP (β = -0.090, P < 0.001), indicating attenuation of genetic effects at higher BMI levels, but not for PP (P = 0.176).
The contrasting interactions of PRS with age (positive) and BMI (negative) reveal fundamentally different mechanisms by which non-modifiable and modifiable factors influence genetic expression. Age amplifies genetic effects particularly on PP, likely reflecting progressive arterial stiffening, while higher BMI attenuates genetic effects through obesity-related mechanisms. These findings suggest that the impact of dietary sodium-potassium balance and genetic risk on BP may vary by age and BMI, warranting consideration in personalized prevention strategies.
