Abstract 560: Vitamin D Depletion Aggravates Hypertension in Transgenic Rats

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Abstract

Introduction: Vitamin D may ameliorate hypertension and kidney disease through genomic and extra-genomic pathways. Several studies have shown that vitamin D levels can affect levels of circulating FoxP3-positive regulatory T-lymphocytes. Previously, our group has demonstrated that adoptive transfer of FoxP3-positive T-lymphocytes ameliorated the phenotype in a mouse model of angiotensin-II induced cardiac damage.

Objective: To investigate the impact of vitamin D depletion in a transgenic rat model of angiotensin II-mediated hypertensive organ failure, and to investigate the possible association with levels of FoxP3 regulatory T-lymphocytes.

Methods: In 4-week old age-matched rats overexpressing the human renin and angiotensinogen genes, group 1 (n=18) received vitamin D depleted chow, and group 2, (n=15) received chow with standard contents of vitamin D. Blood pressure (tail cuff) and 24-hour 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. Lymphocytes from spleens were isolated, and the percentage of CD4+ cells, which were CD4+CD25+FoxP3-positive, was measured by flow cytometry. Mesenteric arteries were removed and stimulated with nitroprusside and acetylcholine to investigate the relaxation potential of the epithelium.

Results: The vitamin D depleted group had higher blood pressure at all times (mean differences were 23.40 mmHg, 14.31 mmHg and 15.71 mmHg respectively, p<0.05), higher heart-to-body weight ratio, and higher ANP and BNP levels. No differences were found between groups in mortality or proteinuria. Neither the levels of CD4+CD25+FoxP3-positive cells in spleen, nor the relaxation potential measured in mesenteric arteries differed between groups.

Conclusion: Short-term vitamin D depletion aggravated hypertension and end-organ damage in a rat model of angiotensin II-induced hypertension. However, the aggravated phenotype was not due to different levels of splenic FoxP3-positive activated T-lymphocytes or to higher endothelial resistance in arteries.

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