Hypertension is a leading global health burden, influenced by both metabolic dysfunction and genetic predisposition. While insulin resistance and visceral adiposity are established contributors, their interplay with genetic factors in hypertension remains incompletely understood. The Metabolic Score for Visceral Fat (METS-VF) provides a validated surrogate for visceral adiposity, yet the genetic architecture of hypertension stratified by METS-VF has not been fully explored.The study aims to investigate the contribution of genetic factors by evaluating the association between single nucleotide polymorphisms (SNPs) and hypertension in populations stratified by METS-VF levels.We analyzed 70,513 participants from the Korean Genome and Epidemiology Study (KoGES). Participants were stratified into tertiles according to METS-VF values, and hypertension prevalence was compared across groups. Genome-wide association studies (GWAS) were performed separately for the lowest (T1) and highest (T3) tertiles, adjusting for age, sex, lifestyle factors. Genome-wide significance was defined as p < 5 × 10⁻⁸. Expression Quantitative Trait Loci (eQTL) analyses were conducted and presented in Supplementary Tables.Hypertension prevalence was substantially higher in the high-risk T3 group (47.3%) compared with the T1 group (14.6%, p < 0.001). GWAS revealed distinct genetic architectures between groups. In T3, 11 loci achieved genome-wide significance, compared with 6 loci in T1. The strongest signals were observed at rs16998073 in FGF5 and rs112735431 in RNF213, both associated with increased hypertension risk across tertiles. Conversely, variants near PRDM8 (rs17004846) and ATP2B1 (rs11105365) demonstrated protective effects. Notably, NT5C2 (rs12416331) was significant only in T1 and has been linked to hyperuricemia, suggesting a uric acid–mediated mechanism. Additional loci included ENPEP, SPTBN1, KCNK3, MYL2, CUX2, and ALDH2.To our knowledge, this is the first study to apply METS-VF to GWAS of hypertension. But, the observational design limits causal inference, and the absence of longitudinal data precludes assessment of temporal relationships.This large-scale GWAS stratified by visceral adiposity identified both shared and unique genetic determinants of hypertension. The findings underscore the modifying effect of visceral fat on genetic associations. Compared with prior METS-IR based analyses, METS-VF may provide a more comprehensive index for integrating metabolic and genetic risk in hypertension.