【摘 要】
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Our earlier study has reported that active vitamin D deficiency in mice causes secondary hypertension and cardiac dysfunction, but underlying mechanism is still largely unknown.To clarify whether exog
【机 构】
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Department of Human Anatomy, Nanjing Medical University,Nanjing, China
【出 处】
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The 18th Congress of the International Federation of Associa
论文部分内容阅读
Our earlier study has reported that active vitamin D deficiency in mice causes secondary hypertension and cardiac dysfunction, but underlying mechanism is still largely unknown.To clarify whether exogenous active vitamin D rescues hypertension and cardiovascular impairment by normalizing overactivation of the central renin-angiotensin system (RAS) via an antioxidative mechanism, 1-alpha-hydroxylase [1 α(OH)ase] gene knockout mice and their wild-type littermates were fed a normal diet or with 1,25-dihydroxy vitamin D3 [1,25(OH)2D3] administration, or a high-calcium, high-phosphorus "rescue" diet with or without the antioxidant N-acetyl-l-cysteine (NAC) supplementation.
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