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Vitamin D Depletion Aggravates Hypertension and Target‐Organ Damage

BACKGROUND: We tested the controversial hypothesis that vitamin D depletion aggravates hypertension and target‐organ damage by influencing renin. METHODS AND RESULTS: Four‐week‐old double‐transgenic rats (dTGR) with excess angiotensin (Ang) II production due to overexpression of the human renin (hRE...

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Detalles Bibliográficos
Autores principales: Andersen, Louise Bjørkholt, Przybyl, Lukasz, Haase, Nadine, von Versen‐Höynck, Frauke, Qadri, Fatimunnisa, Jørgensen, Jan Stener, Sorensen, Grith Lykke, Fruekilde, Palle, Poglitsch, Marko, Szijarto, István, Gollasch, Maik, Peters, Joerg, Muller, Dominik N., Christesen, Henrik Thybo, Dechend, Ralf
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Blackwell Publishing Ltd 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4345870/
https://www.ncbi.nlm.nih.gov/pubmed/25630909
http://dx.doi.org/10.1161/JAHA.114.001417
Descripción
Sumario:BACKGROUND: We tested the controversial hypothesis that vitamin D depletion aggravates hypertension and target‐organ damage by influencing renin. METHODS AND RESULTS: Four‐week‐old double‐transgenic rats (dTGR) with excess angiotensin (Ang) II production due to overexpression of the human renin (hREN) and angiotensinogen (hAGT) genes received vitamin D‐depleted (n=18) or standard chow (n=15) for 3 weeks. The depleted group had very low serum 25‐hydroxyvitamin D levels (mean±SEM; 3.8±0.29 versus 40.6±1.19 nmol/L) and had higher mean systolic BP at week 5 (158±3.5 versus 134.6±3.7 mm Hg, P<0.001), week 6 (176.6±3.3 versus 162.3±3.8 mm Hg, P<0.01), and week 7 (171.6±5.1 versus 155.9±4.3 mm Hg, P<0.05). Vitamin D depletion led to increased relative heart weights and increased serum creatinine concentrations. Furthermore, the mRNAs of natriuretic peptides, neutrophil gelatinase‐associated lipocalin, hREN, and rRen were increased by vitamin D depletion. Regulatory T cells in the spleen and in the circulation were not affected. Ang metabolites, including Ang II and the counter‐regulatory breakdown product Ang 1 to 7, were significantly up‐regulated in the vitamin D‐depleted groups, while ACE‐1 and ACE‐2 activities were not affected. CONCLUSIONS: Short‐term severe vitamin D depletion aggravated hypertension and target‐organ damage in dTGR. Our data suggest that even short‐term severe vitamin D deficiency may directly promote hypertension and impacts on renin‐angiotensin system components that could contribute to target‐organ damage. The findings add to the evidence that vitamin D deficiency could also affect human hypertension.