Sánchez M, de la Sierra A, Coca A, Poch E, Giner V, Urbano-Márquez A
Department of Internal Medicine, Hospital Clínic, University of Barcelona, Spain.
Hypertension. 1997 Jan;29(1 Pt 2):531-6. doi: 10.1161/01.hyp.29.1.531.
We evaluated the effect of oral calcium supplementation on blood pressure, calcium metabolism, and insulin resistance in essential hypertension. After receiving a standard diet with 500 mg of calcium per day during a 4-week period, 20 nondiabetic, essential hypertensive patients were randomized in a double-blind fashion to receive oral calcium supplementation (1500 mg of calcium per day) or placebo for 8 weeks. At the end of the 4-week period of low-calcium diet and after the 8-week period of intervention, we measured blood pressure (by both office and 24-hour ambulatory blood pressure monitoring), calcium-regulating hormones [urinary hydroxyproline and serum osteocalcin, parathormone, and 1,25(OH)2-vitamin D3], intraplatelet free calcium concentration, fasting plasma glucose and insulin levels, and the insulin-sensitivity index (euglycemic-hyperinsulinemic clamp). Compared with patients maintained at low calcium intake, essential hypertensive patients under oral calcium supplementation significantly reduced serum osteocalcin (from 22.2 +/- 1.9 to 17.9 +/- 2.0 micrograms/L; P = .0015), parathormone (from 4.20 +/- 0.38 to 3.30 +/- 0.36 pmol/L; P = .0003), and 1,25(OH)2-vitamin D3 (from 98.0 +/- 11.0 to 61.6 +/- 5.7 pmol/L; P = .0062). Likewise, we found a significant reduction in intraplatelet free calcium concentration (from 35.9 +/- 1.2 to 26.5 +/- 0.8 nmol/L; P = .0005) and fasting plasma insulin levels (from 71.8 +/- 5.9 to 64.6 +/- 6.2 pmol/L; P = .05) and a significant increase in the insulin-sensitivity index (from 2.89 +/- 0.77 to 4.00 +/- 0.95 mg.kg-1.min-1; P = .0007). None of these parameters were significantly modified in patients maintained at low calcium intake. Office and 24-hour mean values of systolic and diastolic blood pressure did not change after 8 weeks of oral calcium supplementation or placebo.
我们评估了口服补钙对原发性高血压患者血压、钙代谢及胰岛素抵抗的影响。20例非糖尿病原发性高血压患者在为期4周的时间里接受每天含500毫克钙的标准饮食，之后被随机分为两组，采用双盲法，一组接受口服补钙（每天1500毫克钙），另一组接受安慰剂，为期8周。在低钙饮食4周结束时以及8周干预期结束后，我们测量了血压（通过诊室血压测量和24小时动态血压监测）、钙调节激素[尿羟脯氨酸、血清骨钙素、甲状旁腺激素及1,25(OH)₂-维生素D₃]、血小板内游离钙浓度、空腹血糖和胰岛素水平以及胰岛素敏感性指数（正常血糖-高胰岛素钳夹技术）。与维持低钙摄入的患者相比，口服补钙的原发性高血压患者血清骨钙素显著降低（从22.2±1.9降至17.9±2.0微克/升；P = 0.0015）、甲状旁腺激素显著降低（从4.20±0.38降至3.30±0.36皮摩尔/升；P = 0.0003）、1,25(OH)₂-维生素D₃显著降低（从98.0±11.0降至61.6±5.7皮摩尔/升；P = 0.0062）。同样，我们发现血小板内游离钙浓度显著降低（从35.9±1.2降至26.5±0.8纳摩尔/升；P = 0.0005）、空腹血浆胰岛素水平显著降低（从71.8±5.9降至64.6±6.2皮摩尔/升；P = 0.05），胰岛素敏感性指数显著升高（从2.89±0.77升至4.00±0.95毫克·千克⁻¹·分钟⁻¹；P = 0.0007）。维持低钙摄入的患者这些参数均无显著变化。口服补钙或安慰剂8周后，诊室收缩压和舒张压的均值以及24小时收缩压和舒张压的均值均未改变。
