BACKGROUND AND OBJECTIVES: The mechanisms underlying racial/ethnic differences in dementia incidence and pathology are multifactorial, and hypertension represents an actionable target for reducing these differences. We aimed to estimate the extent to which controlling for hypertension mediates racial/ethnic inequities in neuroimaging markers of brain aging. METHODS: The Health and Aging Brain Study-Health Disparities cohort is a highly phenotyped, racially and ethnically diverse cohort of cognitive aging. We used marginal structural models with inverse probability weights to estimate total and controlled direct effects of race/ethnicity, hypertension, and systolic blood pressure (SBP) at baseline, with neuroimaging markers measured on average 2 years later. Neuroimaging markers of brain aging were measured at the 2-year follow-up. RESULTS: Among Black and Hispanic participants with any neuroimaging data at the second visit (overall N = 1,347), 68% and 71% were women, 75% and 67% had hypertension, and the mean age was 61 and 63 years, respectively. Black and Hispanic participants had greater white matter hyperintensity volume (WMHV) compared with non-Hispanic White (NHW) participants (n = 1,333, β [95% CI]: Black 2.08 [1.68-2.59], Hispanic 0.99 [0.91-1.08]). After analytically setting hypertension status to absent, Black-NHW inequities in WMHV were attenuated (β [95% CI]: 1.3 [1.01-1.65]). Black participants had lower amyloid deposition compared with NHW participants (n = 679, β [95% CI]: -0.29 [-0.46 to -0.12]), but analytically controlling for hypertension did not appreciably change estimates. Compared with NHW participants, Hispanic participants had lower Alzheimer disease meta-region of interest cortical thickness (n = 1,005, β [95% CI]: -0.20 [-0.34 to -0.07]), but neither hypertension nor SBP significantly mediated this difference. Medial temporal lobe tau-PET standardized uptake value ratio did not significantly differ in Black or Hispanic participants compared with NHW participants (n = 408). DISCUSSION: Black-NHW inequities in subclinical cerebral small vessel disease may be mitigated by population-level efforts to reduce hypertension prevalence. Future studies should extend this work to examine clinical outcomes.