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Introduction Vitamin D may ameliorate hypertension and kidney disease through genomic and extra-genomic pathways. Objective To investigate the impact of vitamin D in a transgenic rat model of angiotensin II-mediated hypertensive organ failure. Methods In 4-week-old age-matched rats overexpressing the human renin and angiotensinogen genes, group 1 ( n = 18) received vitamin D depleted chow; group 2 ( n = 15) standard chow and intraperitoneal paricalcitol at 800 ng/kg thrice weekly; and group 3 ( n = 15) standard chow and vehicle injections. Blood pressure (tail cuff) and 24-h albuminuria were determined once weekly. After three weeks, animals were sacrificed. Heart tissue was examined for atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) by RT-PCR. Results The vitamin D depleted group had higher blood pressure at week 1 (mean difference 23.4 mm Hg, 95% CI 9.1–37.7) and tended to have higher blood pressure in weeks 2 and 3 (mean difference 14.3 mm Hg 95% CI −0.02–28.7 and 15.2 mm Hg 95% CI −1.5–33). The depletion group had higher heart-to-body weight ratio, and a trend towards higher ANP and BNP levels. The group receiving paricalcitol did not perform better. No differences were found between groups in mortality or proteinuria. Conclusion Short-term vitamin D depletion aggravated hypertension and end-organ damage in a rat model of angiotensin II-induced hypertension. Short-term interventions with high-dose vitamin D analogues had no protective effect.