Luft F C, Aronoff G R, Sloan R S, Fineberg N S, Weinberger M H
Clin Pharmacol Ther. 1986 Apr;39(4):414-9. doi: 10.1038/clpt.1986.64.
To test the hypothesis that the supplementation of dietary calcium intake influences sodium homeostasis, the renin-angiotensin system, and sympathetic nervous system in a manner that might evoke a decrease in arterial blood pressure, we gave 16 participants (eight normal and eight with hypertension) placebo for 8 days, followed by 500 mg elemental calcium as the carbonate salt twice a day for 8 days. The same diet was prepared for each meal for the entire study. Sodium intake was fixed for each participant and averaged 150 mEq/day. All urine was collected every day. Blood was drawn at the end of the placebo and calcium periods for determinations of plasma renin, aldosterone, and norepinephrine values. Calcium supplementation increased urinary calcium excretion significantly in both groups. However, calcium supplementation failed to influence sodium or potassium excretion, serum electrolytes, total serum calcium, renin, aldosterone, or norepinephrine levels, or heart rate. Systolic and diastolic blood pressure were not influenced in normal subjects, but in patients with hypertension the supine systolic blood pressure decreased significantly. We conclude that blood pressure lowering effects of calcium, should they occur, are not likely the result of augmented urinary sodium excretion or of straight-forward influences on the renin-angiotensin system or sympathetic nervous system.
为了验证膳食钙摄入量的补充是否会以可能导致动脉血压降低的方式影响钠稳态、肾素 - 血管紧张素系统和交感神经系统，我们让16名参与者（8名正常人和8名高血压患者）服用8天安慰剂，然后每天两次服用500毫克元素钙（碳酸盐形式），持续8天。在整个研究过程中，每餐都准备相同的饮食。为每位参与者固定钠摄入量，平均为150 mEq/天。每天收集所有尿液。在服用安慰剂期和补钙期结束时采集血液，用于测定血浆肾素、醛固酮和去甲肾上腺素值。补钙使两组的尿钙排泄量均显著增加。然而，补钙未能影响钠或钾的排泄、血清电解质、血清总钙、肾素、醛固酮或去甲肾上腺素水平，也未影响心率。正常受试者的收缩压和舒张压未受影响，但高血压患者的仰卧位收缩压显著降低。我们得出结论，钙的降压作用（如果存在的话）不太可能是尿钠排泄增加或对肾素 - 血管紧张素系统或交感神经系统直接影响的结果。
