To evaluate the antihypertensive and hormonal effects of oral magnesium supplementation, 17 inpatients with untreated, uncomplicated mild-to-moderate essential hypertension (EH) and 8 age-matched normotensive controls (controls) were given MgO orally 3 times a day at a daily dose of 1.0 g (0.6 g per day as Mg) for a period of 2 weeks. Supplementation of MgO elicited a significant fall in averaged mean blood pressure calculated with a 24-h ambulatory blood pressure monitoring system (MBP) in EH from a baseline value of 104.3 +/- 12.2 to 99.5 +/- 11.6 mmHg (p < 0.05), while controls remained unaltered from a baseline value of 85.1 +/- 11.5 to 84.5 +/- 13.3 mmHg. The percentage reductions in systolic and diastolic blood pressures were similar during daytime and nighttime in EH. According to the extent of reduction in MBP with magnesium supplementation, EH patients were divided into 2 groups, responder and nonresponder. The level of plasma renin activity (PRA) in the responder group was significantly higher than that of the nonresponder group (p < 0.05). After 2 weeks of magnesium supplementation, the plasma level of Na+, K(+)-ATPase inhibitory activity (PATPI), defined as equivalency to ouabain, was reduced significantly from 0.75 +/- 0.54 to 0.40 +/- 0.30 mumol ouabain/ml (p < 0.05) in the responder group, while it remained unaltered in controls and the nonresponder group. PRA, plasma aldosterone concentration, urinary epinephrine and norepinephrine excretion, and urinary sodium excretion did not change significantly in either control subjects or EH (responder and nonresponder groups). A significant negative correlation existed between the pretreatment PRA and changes in MBP after magnesium supplementation in EH (r = -0.65, p < 0.01), and there was a significant positive correlation between changes in PATPI and changes in MBP as a whole (r = 0.41, p < 0.05). These results support the view that oral magnesium supplementation is a useful approach to treatment of patients with uncomplicated essential hypertension, especially those with high plasmas renin activity. It appears that magnesium suppresses circulating Na+,K(+)-ATPase inhibitory activity to attenuate vascular tone, and thereby reduces blood pressure in EH.
Jpn Heart J 1992 Nov;33(6):785-800