Resnick L
Am J Med. 1986 Dec 15;81(6A):6-14. doi: 10.1016/0002-9343(86)90788-6.
Although abnormalities of calcium metabolism have been described in various hypertensive states, the specific manner in which these abnormalities contribute to the increased pressure remains unclear. Our own group, in attempting to resolve the seemingly contradictory evidence thus far obtained, has adopted an approach emphasizing the clinical as well as biochemical heterogeneity among hypertensive subjects. We have observed the following: broad-based deviations of calcium ionic and hormonal indices in patients with essential hypertension; these deviations are linked with concurrent deviations in the renin-aldosterone system. Thus, low-renin subjects exhibit a calcium ionic and hormonal profile suggestive of calcium deficiency, whereas high-renin subjects have an opposite metabolic profile suggestive of calcium excess; blood pressure responses to dietary salt loading may also differ among renin subgroups of essential hypertension and may be mediated by salt-induced alterations of calcium metabolism. In the absence of these alterations, dietary salt intake results in little or no change in blood pressure; and calcium as a dietary supplement may itself possess antihypertensive properties in targeted subgroups of essential hypertensive patients, preferentially in low-renin, lower ionized calcium subjects. Interestingly, calcium channel blockade also preferentially lowers pressure in low-renin, lower serum ionized calcium forms of hypertension and may define those subjects whose elevated pressure is most dependent on extracellular calcium. Conversely, renin profiling or serum ionized calcium measurements may be used clinically to help target subjects most likely to benefit from calcium channel antagonists. Lastly, unlike other antihypertensive drug classes, high salt intake does not blunt, and may even enhance, the hypotensive effects of calcium channel blockade, lessening the need for stringent dietary recommendations. Altogether, these heterogeneous alterations of calcium metabolism in essential hypertension suggest that the linkage between the regulation of calcium metabolism, renin system activity, and blood pressure in essential hypertension is of pathophysiologic as well as therapeutic relevance.
尽管在各种高血压状态下均已描述了钙代谢异常，但这些异常导致血压升高的具体方式仍不清楚。我们自己的研究小组为了试图解决迄今为止获得的看似矛盾的证据，采用了一种强调高血压患者临床和生化异质性的方法。我们观察到以下情况：原发性高血压患者的钙离子和激素指标存在广泛偏差；这些偏差与肾素 - 醛固酮系统的同时偏差有关。因此，低肾素患者表现出提示钙缺乏的钙离子和激素特征，而高肾素患者则具有相反的提示钙过量的代谢特征；原发性高血压肾素亚组对饮食中盐负荷的血压反应也可能不同，并且可能由盐诱导的钙代谢改变介导。在没有这些改变的情况下，饮食中盐的摄入导致血压几乎没有变化或没有变化；并且钙作为饮食补充剂本身可能在原发性高血压患者的特定亚组中具有降压特性，优先在低肾素、较低离子钙的患者中。有趣的是，钙通道阻滞剂也优先降低低肾素、较低血清离子钙型高血压患者的血压，并且可能确定那些血压升高最依赖细胞外钙的患者。相反，肾素分析或血清离子钙测量可在临床上用于帮助确定最可能从钙通道拮抗剂中获益的患者。最后，与其他抗高血压药物类别不同，高盐摄入不会减弱甚至可能增强钙通道阻滞剂的降压作用，从而减少了严格饮食建议的必要性。总之，原发性高血压中这些钙代谢的异质性改变表明，原发性高血压中钙代谢调节、肾素系统活性和血压之间的联系在病理生理以及治疗方面都具有相关性。
