Lau K, Thomas D, Eby B
Fed Proc. 1986 Nov;45(12):2752-7.
Abnormalities in Ca metabolism in genetic hypertension have been suggested by studies of the spontaneously hypertensive rat and of humans with essential hypertension. A state of relative Ca deficiency in genetic hypertension was previously hypothesized to explain the reduced serum ionized Ca, increased serum parathyroid hormone levels, and the association between oral Ca loading and mild reduction in blood pressure. Renal Ca leak, reduced intestinal Ca absorption, and diminished Ca intake were further postulated to account for the Ca deficient state. This hypothesis, however, is not supported by the following lines of evidence in genetic hypertension: the absence of fasting hypercalciuria owing to intrinsic tubular defects, increased net Ca absorption in vivo despite greater Ca retention before and during established hypertension, increased intracellular free Ca concentrations, the failure to aggravate the hypertension by 50% reduction in dietary Ca intake, and the failure to ameliorate the hypertension by maneuvers that augment Ca balance (parenteral Ca administration, a high Mg diet, and 1,25-dihydroxyvitamin D3 injections). The available literature may be explained by the alternative hypothesis that genetic hypertension is characterized by generalized membrane defects in Ca regulation, resulting in a relative increase in cytosolic free Ca. The mechanism (or mechanisms) and physiological consequences of the disturbances in Ca homeostasis, however, remain to be defined.
对自发性高血压大鼠和原发性高血压患者的研究表明，遗传性高血压患者存在钙代谢异常。先前曾假设遗传性高血压存在相对缺钙状态，以解释血清离子钙降低、血清甲状旁腺激素水平升高，以及口服钙负荷与血压轻度降低之间的关联。进一步推测肾钙泄漏、肠道钙吸收减少和钙摄入量减少是导致缺钙状态的原因。然而，遗传性高血压的以下证据并不支持这一假设：由于内在肾小管缺陷不存在空腹高钙尿症，尽管在高血压确立之前和期间钙潴留增加，但体内净钙吸收增加，细胞内游离钙浓度增加，饮食中钙摄入量减少50%并未加重高血压，以及通过增加钙平衡的措施（静脉注射钙、高镁饮食和注射1,25 - 二羟维生素D3）并未改善高血压。现有文献可以用另一种假说来解释，即遗传性高血压的特征是钙调节存在普遍的膜缺陷，导致细胞质游离钙相对增加。然而，钙稳态紊乱的机制和生理后果仍有待确定。
