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维生素D3与大鼠心血管功能

Vitamin D3 and cardiovascular function in rats.

作者信息

Weishaar R E, Simpson R U

出版信息

J Clin Invest. 1987 Jun;79(6):1706-12. doi: 10.1172/JCI113010.

Abstract

We have previously identified a receptor for 1,25-dihydroxyvitamin D3 in myocardial cells (Simpson, R.U. 1983. Circulation. 68:239.). To establish the relevance of this observation, we evaluated the role of the prohormone vitamin D3 in regulating cardiovascular function. In rats maintained on a vitamin D3-deficient diet for nine weeks, increases in systolic blood pressure (BP) and serum creatine phosphokinase (CPK) were observed. These increases coincided with a reduction of serum calcium from 10.3 to 5.6 mg/dl. However, while serum calcium remained depressed throughout the study, increases in BP and serum CPK were transient. After nine weeks of vitamin D3-depletion, but not after six weeks, ventricular and vascular muscle contractile function were also markedly enhanced. The increase in ventricular contractile function could not be prevented by maintaining serum calcium at 9.0 mg/dl during the period of D3-depletion. These observations suggest a primary role for the vitamin D3-endocrine system in regulating cardiovascular function.

摘要

我们之前已在心肌细胞中鉴定出1,25 - 二羟基维生素D3的一种受体(辛普森,R.U. 1983年。《循环》。68:239)。为确定这一观察结果的相关性,我们评估了激素原维生素D3在调节心血管功能中的作用。在喂食维生素D3缺乏饮食九周的大鼠中,观察到收缩压(BP)和血清肌酸磷酸激酶(CPK)升高。这些升高与血清钙从10.3毫克/分升降至5.6毫克/分升同时出现。然而,尽管在整个研究过程中血清钙一直处于低水平,但血压和血清CPK的升高是短暂的。维生素D3耗竭九周后,而非六周后,心室和血管肌肉的收缩功能也显著增强。在D3耗竭期间将血清钙维持在9.0毫克/分升并不能阻止心室收缩功能的增强。这些观察结果表明维生素D3内分泌系统在调节心血管功能中起主要作用。

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