Get 20M+ Full-Text Papers For Less Than $1.50/day. Start a 7-Day Trial for You or Your Team.

Learn More →

Effects of Oral Magnesium on Blood Pressure and Red Cell Sodium Transport in Patients Receiving Long-term Thiazide Diuretics for Hypertension

Effects of Oral Magnesium on Blood Pressure and Red Cell Sodium Transport in Patients Receiving... Twenty patients receiving long-term (1.0 to 10.3 years) thiazide diuretic treatment for essential hypertension (Th group) received magnesium supplementation as MgO (600 mg Mg/day) for 4 weeks and placebo for another 4 weeks. Before and at the end of each period, we measured blood pressure; intraerythrocyte magnesium, sodium, and potassium (R-Mg, R-Na, and R-K); and erythrocyte ouabain (10-4 M) sensitive sodium efflux rate constant (Kos). The same measurements were also performed in 21 untreated age-matched essential hypertensives (EHT group). In the Th group, R-Mg was lower, R-Na was higher, and Kos was lower than in the EHT group before magnesium supplementation. Oral magnesium resulted in a significant increase in R-Mg (p <0.005) and a decrease in R-Na (p <0.01), together with an increase in Kos (p <0.005) in the Th group. During magnesium supplementation, the increased Kos was correlated negatively with the lowered R-Na (r = −0.57, p <0.01) and positively with the increased R-Mg (r = 0.61, p <0.005). Systolic, diastolic, and mean blood pressures were reduced significantly during magnesium administration by a mean of 7.5, 3.0, and 4.5 mm Hg. The results indicate that long-term diuretic treatment may give rise to an intracellular magnesium deficiency and a suppression in cell membrane active transport for sodium, with a resultant increase in intracellular sodium content. It was also suggested that magnesium supplementation for patients already receiving thiazide diuretics may induce a decrease in intracellular sodium, possibly through an activation of Na-K-ATPase, which in turn may contribute to the further reduction in blood pressure. Am J Hypertens 1988;1:71S–74S http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png American Journal of Hypertension Oxford University Press

Effects of Oral Magnesium on Blood Pressure and Red Cell Sodium Transport in Patients Receiving Long-term Thiazide Diuretics for Hypertension

Loading next page...
 
/lp/oxford-university-press/effects-of-oral-magnesium-on-blood-pressure-and-red-cell-sodium-DVXxZEJSL4

References (0)

References for this paper are not available at this time. We will be adding them shortly, thank you for your patience.

Publisher
Oxford University Press
Copyright
© 1988 by the American Journal of Hypertension, Ltd.
ISSN
0895-7061
eISSN
1941-7225
DOI
10.1093/ajh/1.3.71S
Publisher site
See Article on Publisher Site

Abstract

Twenty patients receiving long-term (1.0 to 10.3 years) thiazide diuretic treatment for essential hypertension (Th group) received magnesium supplementation as MgO (600 mg Mg/day) for 4 weeks and placebo for another 4 weeks. Before and at the end of each period, we measured blood pressure; intraerythrocyte magnesium, sodium, and potassium (R-Mg, R-Na, and R-K); and erythrocyte ouabain (10-4 M) sensitive sodium efflux rate constant (Kos). The same measurements were also performed in 21 untreated age-matched essential hypertensives (EHT group). In the Th group, R-Mg was lower, R-Na was higher, and Kos was lower than in the EHT group before magnesium supplementation. Oral magnesium resulted in a significant increase in R-Mg (p <0.005) and a decrease in R-Na (p <0.01), together with an increase in Kos (p <0.005) in the Th group. During magnesium supplementation, the increased Kos was correlated negatively with the lowered R-Na (r = −0.57, p <0.01) and positively with the increased R-Mg (r = 0.61, p <0.005). Systolic, diastolic, and mean blood pressures were reduced significantly during magnesium administration by a mean of 7.5, 3.0, and 4.5 mm Hg. The results indicate that long-term diuretic treatment may give rise to an intracellular magnesium deficiency and a suppression in cell membrane active transport for sodium, with a resultant increase in intracellular sodium content. It was also suggested that magnesium supplementation for patients already receiving thiazide diuretics may induce a decrease in intracellular sodium, possibly through an activation of Na-K-ATPase, which in turn may contribute to the further reduction in blood pressure. Am J Hypertens 1988;1:71S–74S

Journal

American Journal of HypertensionOxford University Press

Published: Jul 1, 1988

There are no references for this article.