Journal
NEUROSCIENCE LETTERS
Volume 588, Issue -, Pages 184-189Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2015.01.013
Keywords
Central nervous system; Hypertension; Oxidative stress; Renin-angiotensin system; Vitamin D; 1-Alpha-hydroxylase knockout
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Funding
- National Natural Science Foundation of China [81200184]
- Natural Science Research Project of Jiangsu Provincial Universities, China [11KJB310004]
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Previously, we reported that active vitamin D deficiency in mice causes secondary hypertension and cardiac dysfunction, but the underlying mechanism remains largely unknown. To clarify whether exogenous active vitamin D rescues hypertension by normalizing the altered central renin-angiotensin system (RAS) via an antioxidative stress mechanism, 1-alpha-hydroxylase [1 alpha(OH)ase] knockout mice [1 alpha(OH)ase(-/-)] and their wild-type littermates were fed a normal diet alone or with 1,25-dihydroxyvitamin D-3 [1,25(OH)(2)D-3], or a high-calcium, high-phosphorus rescue diet with or without antioxidant N-acetyl-L-cysteine (NAC) supplementation for 4 weeks. Compared with their wild-type littermates, 1 alpha(OH)ase(-/-)mice had high mean arterial pressure, increased levels of renin, angiotensin II (Ang II), and Ang II type 1 receptor, and increased malondialdehyde levels, but decreased anti-peroxiredoxin I and IV proteins and the antioxidative genes glutathione reductase (Gsr) and glutathione peroxidase 4 (Gpx4) in the brain samples. Except Ang II type 1 receptor, these pathophysiological changes were rescued by exogenous 1,25(OH)(2)D-3 or NAC plus rescue diet, but not by rescue diet alone. We conclude that 1,25(OH)(2)D-3 normalizes the altered central RAS in 1 alpha(OH)ase(-/-)mice, at least partially, through a central antioxidative mechanism. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
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