Af. Sanjuliani et al., EFFECTS OF MAGNESIUM ON BLOOD-PRESSURE AND INTRACELLULAR ION LEVELS OF BRAZILIAN HYPERTENSIVE PATIENTS, International journal of cardiology, 56(2), 1996, pp. 177-183
Fifteen patients with uncomplicated mild to moderate primary hypertens
ion (7 males, 8 females, age range 36-65 years) were submitted to a do
uble 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 peri
od of 6 weeks. This was to test the effects of oral magnesium suppleme
ntation on blood pressure and sodium, potassium, calcium and magnesium
intraerythrocyte concentrations. Concomitantly, plasma renin activity
and serum aldosterone was also measured. Oral magnesium reduced signi
ficantly 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 concen
tration was reduced (Delta = -0.55 mEq/l per cell, P < 0.01) and intra
erythrocyte magnesium concentration was increased (Delta = 1.20 mg/dl
per cell, P < 0.01). The diminution of the blood pressure correlated p
ositively 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 percen
t of our patients had their blood pressure effectively controlled (mor
e than 10 mmHg reduction in mean blood pressure), being the hypotensiv
e effect more evident in patients with recent hypertension and in thos
e where the reduction in intraerythrocyte sodium was significantly gre
ater than in the non-responder individuals. Intraerythrocyte potassium
and calcium, serum aldosterone, plasma renin activity and urinary sod
ium excretion were maintained unchanged after magnesium supplementatio
n. These data showed that oral magnesium supplementation may reduce th
e blood pressure, which can be partially explained by the decrease in
intracellular sodium and augment in intracellular magnesium.