Resnick L M
Cardiovascular Center, The New York Hospital-Cornell University Medical Center, New York 10021.
Adv Second Messenger Phosphoprotein Res. 1990;24:535-41.
On the basis of this work, we believe it is reasonable to suggest that calcium regulating hormones in general, and 1,25 dihydroxyvitamin D in particular, contribute to the pathophysiology of human essential hypertension, especially salt sensitive forms. As such, levels of plasma renin activity, circulating ionized calcium, and serum 1,25 D levels both contribute to and serve as predictors of dietary salt-sensitivity and the potential benefit of increased oral calcium intake. Mechanistically, the different metabolic set points of these factors, determined on a genetic and/or environmental basis, serve to determine the heterogeneous blood pressure responses to similar dietary and mineral intakes. In this scheme, these monovalent and divalent ion regulating hormones transduce environmental mineral signals at the cellular level, thus determining their ultimate blood pressure effects. The cellular mechanism by which these altered metabolic hormonal set points serve to shift levels of intracellular cytosolic free calcium and other critical determinants of blood pressure, are the focus of current research.
基于这项研究，我们认为有理由提出，一般的钙调节激素，特别是1,25-二羟基维生素D，参与了人类原发性高血压的病理生理过程，尤其是盐敏感性高血压。因此，血浆肾素活性、循环离子钙水平和血清1,25-D水平既参与了饮食盐敏感性的形成，又可作为其预测指标，同时也是增加口服钙摄入量潜在益处的预测指标。从机制上讲，这些因素在遗传和/或环境基础上所确定的不同代谢设定点，决定了对相似饮食和矿物质摄入的异质性血压反应。在这个模式中，这些单价和二价离子调节激素在细胞水平上传递环境矿物质信号，从而决定它们最终的血压效应。这些改变的代谢激素设定点通过何种细胞机制来改变细胞内游离钙离子水平以及其他血压关键决定因素，是当前研究的重点。
