Resnick L M
Can J Physiol Pharmacol. 1986 Jun;64(6):803-7. doi: 10.1139/y86-137.
Alterations of calcium metabolism in hypertensive disease have been increasingly observed, although the specific manner in which these alterations contribute to the increased blood pressure remains unclear. We have studied calcium metabolism in essential hypertension and have adopted an approach based on analysis of renin system activity, which emphasizes the heterogeneity of human hypertensive disease. With this approach we have defined parallel deviations of plasma renin activity, circulating ionized calcium, and calcium-regulating hormones, which suggest a calcium deficiency in some hypertensives and, an excess of calcium in others. These deviations can be used to predict and may mediate the blood pressure sensitivity of hypertensives to dietary salt, and may also target those individuals most likely to benefit from oral calcium supplementation. Calcium itself has enhanced antihypertensive effects in low renin subjects, having lower ionized calcium and higher endogenous 1,25-dihydroxyvitamin D values, and in subjects on higher dietary salt intakes. Calcium may alter pressure, at least in part, by suppressing endogenous vitamin D metabolites and by stimulating calcitonin secretion. We hypothesize that calcium-regulating hormones participate in the physiology of the renin-angiotensin system and in the pathophysiology of human hypertension.
尽管高血压疾病中钙代谢的改变日益受到关注，但这些改变导致血压升高的具体机制仍不清楚。我们对原发性高血压患者的钙代谢进行了研究，并采用了一种基于肾素系统活性分析的方法，该方法强调了人类高血压疾病的异质性。通过这种方法，我们确定了血浆肾素活性、循环离子钙和钙调节激素的平行偏差，这表明一些高血压患者存在钙缺乏，而另一些患者则存在钙过量。这些偏差可用于预测高血压患者对饮食中盐的血压敏感性，并可能介导这种敏感性，还可以针对那些最可能从口服补钙中受益的个体。钙本身对低肾素患者（其离子钙较低且内源性1,25-二羟维生素D值较高）以及高盐饮食患者具有增强的降压作用。钙可能至少部分通过抑制内源性维生素D代谢产物和刺激降钙素分泌来改变血压。我们推测钙调节激素参与肾素-血管紧张素系统的生理过程以及人类高血压的病理生理过程。
