Sanjuliani A F, de Abreu Fagundes V G, Francischetti E A
CLINEX Clinical and Experimental Pathophysiological Center, Rio de Janeiro State University, Brazil.
Int J Cardiol. 1996 Oct 11;56(2):177-83. doi: 10.1016/0167-5273(96)02716-7.
Fifteen patients with uncomplicated mild to moderate primary hypertension (7 males, 8 females, age range 36-65 years) were submitted to a double blind randomized crossover study, receiving MgO 3 times a day at a daily dose of 1.0 g (600 mg/day of magnesium) and placebo for a period of 6 weeks. This was to test the effects of oral magnesium supplementation on blood pressure and sodium, potassium, calcium and magnesium intraerythrocyte concentrations. Concomitantly, plasma renin activity and serum aldosterone was also measured. Oral magnesium reduced significantly the systolic (delta = -7.6 mmHg, P < 0.05); diastolic (delta = -3.8 mmHg, P < 0.01) and mean blood pressure (delta = -5.9 mmHg, P < 0.01). After magnesium supplementation intraerythrocyte sodium concentration was reduced (delta = -0.55 mEq/l per cell, P < 0.01) and intraerythrocyte magnesium concentration was increased (delta = 1.20 mg/dl per cell, P < 0.01). The diminution of the blood pressure correlated positively with the reduction in intraerythrocyte sodium (r = 0.66, P < 0.01) after magnesium. However, our results have shown that the blood pressure response to oral magnesium was not homogeneous. Forty percent of our patients had their blood pressure effectively controlled (more than 10 mmHg reduction in mean blood pressure), being the hypotensive effect more evident in patients with recent hypertension and in those where the reduction in intraerythrocyte sodium was significantly greater than in the non-responder individuals. Intraerythrocyte potassium and calcium, serum aldosterone, plasma renin activity and urinary sodium excretion were maintained unchanged after magnesium supplementation. These data showed that oral magnesium supplementation may reduce the blood pressure, which can be partially explained by the decrease in intracellular sodium and augment in intracellular magnesium.
15例无并发症的轻度至中度原发性高血压患者（7例男性，8例女性，年龄范围36 - 65岁）接受了一项双盲随机交叉研究，每天3次服用氧化镁，每日剂量为1.0 g（相当于每日补充镁600 mg），并服用安慰剂，为期6周。目的是测试口服补充镁对血压以及红细胞内钠、钾、钙和镁浓度的影响。同时，还测量了血浆肾素活性和血清醛固酮。口服镁显著降低了收缩压（差值 = -7.6 mmHg，P < 0.05）；舒张压（差值 = -3.8 mmHg，P < 0.01）和平均血压（差值 = -5.9 mmHg，P < 0.01）。补充镁后红细胞内钠浓度降低（差值 = -0.55 mEq/l/细胞，P < 0.01），红细胞内镁浓度升高（差值 = 1.20 mg/dl/细胞，P < 0.01）。补充镁后血压的降低与红细胞内钠的减少呈正相关（r = 0.66，P < 0.01）。然而，我们的结果表明，口服镁对血压的反应并不一致。40%的患者血压得到有效控制（平均血压降低超过10 mmHg），降压效果在近期高血压患者以及红细胞内钠减少明显大于无反应个体的患者中更为明显。补充镁后红细胞内钾和钙、血清醛固酮、血浆肾素活性和尿钠排泄均保持不变。这些数据表明，口服补充镁可能降低血压，这部分可以通过细胞内钠的减少和细胞内镁的增加来解释。
