Intraerythrocyte Sodium Content Research Articles

Inhibitory Effect of Fluoride on Na+,K+ ATPase Activity in Human Erythrocyte Membrane.

The present study was performed to evaluate the role of long-term consumption of excessive fluoride on electrolyte homeostasis and their transporting mechanisms in erythrocytes of subjects afflicted with dental and skeletal fluorosis. A total of 620 adult (20-50 years) Indian residents participated in this study: 258 men and 242 women exposed to high concentrations of fluoride and 120 age and gender-matched control subjects. Erythrocytes were isolated from blood samples, washed, and used for the estimation of intraerythrocyte sodium and potassium concentrations. Na+,K+ ATPase activity was determined spectrophotometrically from a ghost erythrocyte membrane prepared by osmotic lysis. Erythrocyte analytes were correlated with the water and serum fluoride concentrations by Pearson's bivariate correlation and regression analysis. Results indicated a significant increase in intraerythrocyte sodium (F=14306.265, P<0.0001) in subjects from endemic fluorosis study groups as compared to controls. A significant (P<0.05) positive correlation of intracellular sodium was found with water and serum fluoride concentrations. Mean concentration of intraerythrocytic potassium ions showed significant reduction (F=9136.318, P<0.0001) in subjects exposed to fluoride. A significant (P<0.05) negative correlation of potassium ions was noted with water and serum fluoride concentrations. Na+,K+ ATPase activity was significantly declined (F=1572.763, P<0.0001) in subjects exposed to fluoride. A significant (P<0.05) inverse relationship of Na+,K+ ATPase activity was revealed with water and serum fluoride concentrations.

Inhibitory effect of insulin on vasopressin-induced intracellular calcium response is blunted in hyperinsulinemic hypertensive patients: role of membrane fatty acid composition

Impaired insulin-mediated vasodilation has been implicated in hypertension that is associated with the metabolic syndrome. The aim of this study was to determine whether an abnormality in membrane fatty acid composition was related to a weakening of insulin's inhibitory effect on agonist-stimulated intracellular free calcium elevation. Mild to moderate hypertensive patients (n = 27) and normotensive controls (n = 11) were studied. Hypertensive patients were divided into normoinsulinemic patients (n = 14) and hyperinsulinemic patients (n = 13) according to the area under the curve of plasma insulin concentrations during a 75-g oral glucose tolerance test. Nonstimulated and arginine-vasopressin (AVP) (1 micromol/l)-stimulated intraplatelet free calcium concentrations (p[Ca(2+)](i)) were measured with or without insulin (100 microU/ml) preincubation. Platelet membrane fatty acid composition, intraerythrocyte sodium content, and the ouabain-sensitive sodium efflux rate constant (K (os)) of erythrocytes were also determined. Insulin preincubation reduced AVP-stimulated p[Ca(2+)](i) elevation in both normotensive controls and hypertensive patients. The inhibitory effect of insulin on AVP-stimulated elevation of p[Ca(2+)](i) (%Inhibition) was significantly (P < 0.05) blunted in hyperinsulinemic hypertensive patients (9.7% +/- 2.4%) as compared to normoinsulinemic hypertensive patients (17.4% +/- 2.7%) and normotensive controls (16.9% +/- 1.7%). In hypertensive patients, the %Inhibition was correlated negatively with saturated fatty acids (SFA) (r = -0.51, P < 0.05) and systolic blood pressure (r = -0.44, P < 0.05), and correlated positively with membrane polyunsaturated fatty acids (PUFA) (r = 0.53, P < 0.01) and K (os) (r = 0.53, P < 0.005). Multiple regression analysis showed that SFA, PUFA, and K (os) were the significant variables for %Inhibition. These findings indicate that an increase in SFA and a decrease in PUFA may cause insulin insensitivity in cellular calcium and sodium handling in hypertension with hyperinsulinemia.

Leptin, obesity, insulin resistance and intraerythrocyte sodium content in hypertensive syndrome

Leptin, obesity, insulin resistance and intraerythrocyte sodium content in hypertensive syndrome

Effects of magnesium on blood pressure and intracellular ion levels of Brazilian hypertensive patients

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 (Δ = −7.6 mmHg, P < 0.05); diastolic (Δ = −3.8 mmHg, P < 0.01) and mean blood pressure (Δ = −5.9 mmHg, P < 0.01). After magnesium supplementation intraerythrocyte sodium concentration was reduced (Δ = −0.55 mEq/l per cell, P < 0.01) and intraerythrocyte magnesium concentration was increased (Δ = 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.

Effects of magnesium on blood pressure and intracellular ion levels of Brazilian hypertensive patients

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 (Δ = −7.6 mmHg, P < 0.05); diastolic (Δ = −3.8 mmHg, P < 0.01) and mean blood pressure (Δ = −5.9 mmHg, P < 0.01). After magnesium supplementation intraerythrocyte sodium concentration was reduced (Δ = −0.55 mEq/l per cell, P < 0.01) and intraerythrocyte magnesium concentration was increased (Δ = 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.

Cellular Sodium Transport in Severe Preeclampsia and Chronic Hypertension During Pregnancy

Background: There are contrasting reports on cation transport during hypertensive pregnancies, with either increased or decreased sodium-potassium pump function compared to normotensive pregnancies.Methods: Intraerythrocyte sodium and potassium content as well as transmembrane sodium transport were investigated in the third trimester in normotensive (n = 11), chronic hypertensive (n = 16), and severe preeclamptic (n = 6) pregnancies.Results: There was a significant decrease in intraerythrocyte potassium content and in sodium efflux rate constant in the severe preeclamptic women. There was no difference between the two hypertensive groups in intraerythrocyte sodium content during pregnancy. Ten of the women with chronic hypertension were followed sequentially at gestational week 24, 30, and 36; and 10 hypertensive women were also studied postpartum. There was a significant decrease in intraerythrocyte sodium and an increasing sodium efflux rate constant with increasing gestational age. When studied postpar...

Erythrocyte Sodium-Potassium Transport in Cystic Fibrosis

Erythrocytes from 15 patients with cystic fibrosis (CF) aged 8 mo to 22 y (mean age 12.8 y) were analyzed for Na+,K(+)-ATPase activity and sodium, potassium, and ATP concentrations. Sodium concentrations and Na(+)-K+ ratio of erythrocytes were statistically significantly lower in the CF patients [6.6 (SD 1.9) versus 9.2 (SD 1.1) mmol/L (p less than 0.01) and 0.070 (SD 0.023) versus 0.104 (SD 0.016) mmol/L (p less than 0.01), respectively]. The Na+,K(+)-ATPase activity was similar compared with that of reference individuals [536 (SD 100) versus 488 (SD 92) nmol inorganic phosphate/mg protein/h]. Intraerythrocyte sodium concentration and Na(+)-K+ ratio were thus lower in relation to the recorded Na+,K(+)-ATPase activities in controls, indicating a change of the passive transmembrane movements of sodium ions in CF. There was a rise of erythrocyte sodium and Na(+)-K+ ratio despite unchanged Na+,K(+)-ATPase activity after regular infusion of a fat emulsion rich in essential fatty acids, inferring that an altered membrane composition by essential fatty acid deficiency could explain the low intracellular sodium concentration in CF.

Magnesium supplementation prevents the development of alcohol-induced hypertension.

The effect of chronic alcohol administration on blood pressure was investigated in 7-week-old Wistar rats. Tail-cuff blood pressure was significantly higher in rats who received 15% ethanol in drinking water than in control rats. Intracellular free calcium concentration of lymphocytes was increased, while magnesium concentration of erythrocyte, aorta, and skeletal muscle and erythrocyte ouabain-sensitive 22Na efflux rate constant (Kos) were decreased in alcohol-induced hypertensive rats but not in control rats. Extracellular fluid volume was also increased in alcohol-administered rats. Oral magnesium supplementation (1% MgO in rat chow) attenuated the development of alcohol-induced hypertension accompanied by increased magnesium concentration of erythrocyte, aorta, skeletal muscle, and Kos and decreased intraerythrocyte sodium concentration. Norepinephrine half-life time of the heart and spleen was also increased in magnesium-supplemented rats. Blood pressure significantly correlated positively with intracellular calcium concentration and extracellular fluid volume, negatively with magnesium concentration of erythrocyte, aorta, skeletal muscle, and Kos. These results suggest that increased intracellular calcium, which was partly due to magnesium depletion and suppressed sodium pump activity, and expanded body fluid volume had a possible role in the development of alcohol-induced hypertension. It is also suggested that oral magnesium supplementation had a hypotensive effect on alcohol-induced hypertension possibly through decreased intracellular sodium concentration caused by an activation of sodium pump and decreased sympathetic nervous activity.

Thein vitroEffects of Griffonin and Ouabain on Erythrocyte Sodium Content Obtained from Normal Subjects and Sickle Cell Patients

The in vitro effects of griffonin and ouabain on erythrocyte sodium content have been investigated in 6 normal subjects and 6 sickle cell patients. Intracellular sodium contents of normal or sickle cells incubated for 8 h in tris buffer, griffonin/tris buffer, or ouabain/tris buffer were determined. Incubation of normal cells in tris buffer or 0.5 mmol/l griffonin had little effect on the cell sodium content. However, 1.0 mmol/l griffonin/tris buffer raised the cell sodium level (P less than 0.05) over the incubation period. Ouabain/tris buffer (0.5 mmol/l or 1.0 mmol/l) also raised the sodium content (P less than 0.05 to P less than 0.001). Incubation of sickle cells in tris buffer raised the cell sodium (P less than 0.05) as did 0.5 mmol/l or 1.0 mmol/l griffonin (P less than 0.05 to P less than 0.001). Ouabain/tris buffer (0.5 mmol/l or 1.0 mmol/l) raised the intra-erythrocyte sodium level (P less than 0.01 to P less than 0.001). These findings suggest that ouabain and griffonin both have similar actions on intra-erythrocyte sodium content although ouabain was more potent. It is suggested therefore that griffonin could be a useful anti-sickling drug for sickle cell disease crisis.

The Effect of Ca and Mg Supplementation and the Role of the Opioidergic System on the Development of DOCA-Salt Hypertension

The effect of calcium and magnesium supplementation and the role of opioidergic system was examined in deoxycorticosterone acetate (DOCA)-salt hypertensive rats. The rats were divided into four groups receiving standard laboratory rat diet (control group; n = 9); a calcium-rich diet with 2% CaCl2 added (Ca-group; n = 12); a magnesium-rich diet with 0.5% MgO added (Mg-group; n = 11); and a calcium and magnesium-rich diet with 2% CaCl2 and 0.5% MgO added (Ca/Mg-group; n = 11); each diet contained 7% NaCl. After four weeks on these diets, the rats were decapitated and blood was obtained for the measurement of plasma electrolytes, intraerythrocyte sodium, potassium and magnesium content (RBC-Na, -K, in mEq/L cells and RBC-Mg, in mg/dL cells) and plasma beta-endorphin concentration (beta-END, in pg/mL). In the control group, systolic blood pressure and RBC-Na were obviously higher than in the other groups. Plasma beta-endorphin concentration was 45.1 +/- 13.4 in the control group, 70.7 +/- 17.4 in the Ca-group (P less than .05 v control group), 58.0 +/- 20.1 in the Mg-group and 83.8 +/- 24.8 in the Ca/Mg-group (P less than .01 v control group). The blood pressure correlated significantly with both RBC-Na (r = 0.416, P less than .01) and beta-END (r = 0.436, P less than .005). A negative correlation was also observed between RBC-Na and beta-END (r = 0.437, P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)

Normotensive young men with family histories of hypertension gain weight and decrease their intraerythrocyte sodium content during a 5‐year follow‐up

Young normotensive men matched for age and body mass index with (n = 16) and without (n = 13) family histories of hypertension were investigated at baseline and after 5 years of follow-up with respect to blood pressure, body weight and intracellular sodium content. Subjects with positive family histories of hypertension increased significantly in body weight (from 81.9 +/- 11.5 kg to 89.5 +/- 11.4 kg, P less than 0.001) compared to subjects with negative family histories of hypertension (from 79.9 +/- 10.8 kg to 80.7 +/- 12.2 kg, NS). Their blood pressure did not differ initially (137 +/- 12/75 +/- 11 mmHg vs. 135 +/- 8/72 +/- 9 mmHg), but was reduced in subjects without family histories of hypertension (to 125 +/- 3/68 +/- 13 mmHg) in the follow-up examination. At follow-up, body mass index showed a positive correlation with blood pressure among subjects with positive family histories of hypertension (r = 0.77, P less than 0.001). At baseline, subjects with hypertensive fathers had significantly higher intraerythrocyte sodium levels than subjects with normotensive parents. At re-examination 5 years later, this difference was no longer present. We conclude that normotensive subjects with positive family histories of hypertension are predisposed to gain weight rather than to show an increase in blood pressure at this age. Normalization of intracellular sodium content, as found in the present study, could be a consequence of this weight gain and the ensuing metabolic adaption.

Renal sodium handling and sodium transport inhibitor in salt-sensitive essential hypertension

To investigate the mechanism whereby blood pressure rises with NaCl loading in salt-sensitive essential hypertension, salt-sensitivity index was determined along with sodium and lithium clearances, plasma Na+,K(+)-ATPase inhibitor and intra-erythrocyte sodium and potassium concentrations. Salt-sensitivity index was defined as the percentage of change in mean blood pressure when NaCl intake was changed from low (34 mmol/day) to high (342 mmol/day). Salt-sensitivity index was inversely correlated with fractional excretion of lithium both on the low and high NaCl diets (r = -0.721, P less than 0.01 and r = -0.591, P less than 0.02, respectively; n = 16), but not with fractional excretion of sodium. The change of plasma Na+,K(+)-ATPase inhibition with NaCl loading had a direct correlation with salt-sensitivity index (r = 0.704, P less than 0.01; n = 16). Either intra-erythrocyte sodium and potassium concentrations or the ratio of these two values did not change significantly with an increase of dietary NaCl intake. These results suggest that an enhancement of proximal tubular sodium reabsorption stimulates secretion of plasma Na+,K(+)-ATPase inhibitor which may be involved in a rise in blood pressure with sodium loading. They also suggest that lithium clearance is a determinant which can predict salt sensitivity without actual NaCl loading.

Renal sodium handling and sodium transport inhibitor in salt-sensitive essential hypertension

To investigate the mechanism whereby blood pressure rises with NaCl loading in salt-sensitive essential hypertension, salt-sensitivity index was determined along with sodium and lithium clearances, plasma Na+,K(+)-ATPase inhibitor and intra-erythrocyte sodium and potassium concentrations. Salt-sensitivity index was defined as the percentage of change in mean blood pressure when NaCl intake was changed from low (34 mmol/day) to high (342 mmol/day). Salt-sensitivity index was inversely correlated with fractional excretion of lithium both on the low and high NaCl diets (r = -0.721, P less than 0.01 and r = -0.591, P less than 0.02, respectively; n = 16), but not with fractional excretion of sodium. The change of plasma Na+,K(+)-ATPase inhibition with NaCl loading had a direct correlation with salt-sensitivity index (r = 0.704, P less than 0.01; n = 16). Either intra-erythrocyte sodium and potassium concentrations or the ratio of these two values did not change significantly with an increase of dietary NaCl intake. These results suggest that an enhancement of proximal tubular sodium reabsorption stimulates secretion of plasma Na+,K(+)-ATPase inhibitor which may be involved in a rise in blood pressure with sodium loading. They also suggest that lithium clearance is a determinant which can predict salt sensitivity without actual NaCl loading.

Role of Intracellular Cation Abnormalities in Development of Left Ventricular Hypertrophy

To elucidate factors determining the development of left ventricular hypertrophy, we performed measurements of intraerythrocyte sodium and intraplatelet calcium concentrations, measurements of plasma and urinary catecholamine levels and plasma renin activity, calculation of left ventricular mass using echocardiography, and 24-h ambulatory blood pressure (BP) monitoring. The results indicate that abnormalities of sodium and calcium mobilization may play an important role in the adaptation of left ventricular muscle to a persistent increase in BP.

Erythrocyte concentrations and transmembrane fluxes of sodium and potassium in essential hypertension: Role of intrinsic and environmental factors

The intraerythrocyte sodium concentration is increased in the erythrocytes of Zaïrean Bantu with untreated hypertension, while the red blood cell potassium is not different from that of normotensive subjects. Compared with whites, normotensive healthy blacks have a higher intracellular concentration of sodium due to a depressed activity of the sodium-potassium pump. Normotensive healthy males with a positive familial background of hypertension display higher erythrocyte sodium and lower cotransport activity. None of the two measurements offer a clear-cut genetic marker of essential hypertension. In healthy women, the erythrocyte sodium concentration is lowered during the luteal as compared with the follicular phase of the menstrual cycle. This variability explains the difference observed between men and women. A low-sodium diet stimulates the activity of the sodium-potassium ATPase pump, which leads to a decrease in the erythrocyte sodium concentration. Both alterations reverse only slowly during sodium repletion. It is therefore suggested that an adequate matching for race, sex, stage of the menstrual cycle (in women), family history of hypertension, and the amount of sodium in the diet should be a prerequisite for valid conclusions when interpreting the erythrocyte concentration and fluxes of sodium.

Dietary linoleic acid prevents the development of deoxycorticosterone acetate-salt hypertension.

The aim of this study was to elucidate the effect of dietary variations of linoleic acid on the development of deoxycorticosterone acetate (DOCA)-salt hypertension in rats. All rats were divided into three groups and fed one of the following isocaloric diets with 8% NaCl: a high linoleic acid (HLA) (20% sunflower oil), a moderate linoleic acid (5% lard oil + 15% sunflower oil), or a low linoleic acid (DLA) (20% lard oil). After 4 weeks of feeding, we determined intraerythrocyte sodium, potassium, and magnesium concentrations, intra-aortic and lymphocyte magnesium content, and erythrocyte ouabain-sensitive 22Na efflux rate constant. Cytoplasmic free calcium concentration of lymphocytes from thymus was also determined with quin-2 as a fluorescent indicator. In the HLA group, the elevation of systolic blood pressure was significantly attenuated, and intraerythrocyte sodium concentration was significantly lower than in the DLA group. There were greater intraerythrocyte potassium and magnesium concentrations, intra-aortic and lymphocyte magnesium contents, and erythrocyte ouabain-sensitive 22Na efflux rate constant in the HLA group as compared with other groups. Cytoplasmic free calcium concentration in the HLA group was significantly lower than in other groups. Systolic blood pressure significantly correlated negatively with intraerythrocyte and intra-aortic magnesium concentrations and intraerythrocyte potassium concentration, and correlated positively with cytoplasmic free calcium concentration. Erythrocyte ouabain-sensitive 22Na efflux rate constant significantly correlated positively with intraerythrocyte magnesium concentration. These findings suggest that dietary linoleic acid can attenuate the development of DOCA-salt hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of acute vascular fluid volume expansion on erythrocyte sodium transport in essential hypertension

Evidence exists that volume expansion is associated with the appearance of a circulating sodium transport inhibitor. We have evaluated intra-arterial blood pressure (BP), central venous pressure (CVP), plasma renin activity (PRA), intraerythrocyte sodium content, erythrocyte sodium influx and rate constant of sodium efflux in 10 untreated primary hypertensive men (WHO stages I and II). The investigations were done during baseline conditions and after rapid intravenous infusion of 1 litre of saline (0.9% NaCl solution) over 15-20 min. Volume expansion caused an increase in CVP by 6.0 +/- 0.5 cmH2O (p less than 0.01), while BP only exhibited a slight increase. No significant changes in intraerythrocyte sodium content, sodium influx, sodium efflux rate constant or PRA were found after volume expansion compared to baseline. All patients with low normal PRA experienced a decrease in sodium efflux rate constant after volume expansion. We found a positive correlation between baseline PRA and change in sodium efflux rate constant after volume expansion (r = 0.62, p less than 0.05). At baseline the relationship between PRA and intraerythrocyte sodium content nearly reached statistical significance (r = 0.63, p = 0.054). These results may indicate that acute volume expansion influences the release of a circulating factor, modulating sodium transport in low-renin hypertension.

Increase in plasma digitalis-like activity during percutaneous transluminal coronary angioplasty in patients with coronary stenosis

Despite the fact that numerous studies have been published regarding the possible presence in plasma of an endogenous NaK pump inhibitor with a digitalis-like structure in essential hypertension, very little is known about this factor in heart disease in general, and in situations characterized by low cardiac output. We measured the ability of plasma obtained from the femoral vein to inhibit a human renal Na +K + ATPase before and immediately after percutaneous transluminal coronary angioplasty (PTCA) in 6 patients suffering from angina pectoris and severe coronary stenosis. Intraerythrocyte sodium and potassium concentrations were also measured simultaneously. Na +-K + ATPase inhibition proved significantly greater after angioplasty as compared to basal activity (percentage inhibition: 31.5 ± 7.8 vs 16.1 ± 12.2). No significant changes in intraerythrocyte sodium and pottasium were detected. Though we are not in a position to define the mechanism underlying the increase in the digitalis-like factor, a plausible hypothesis may be that the reduction in cardiac output during PTCA by raising cardiac pressures may stimulate the production of a factor of compensatory inotropic significance.

Assessment of the NMR visibility of intraerythrocytic sodium by flame photometric and ion-competitive studies.

23Na nuclear magnetic resonance (NMR) studies of intraerythrocytic sodium concentrations were performed at 37 degrees C and the accuracy of the method was evaluated through concomitant emission flame photometric analysis. NMR visibility of intraerythrocytic sodium was estimated to be 75 +/- 3%. Verification of the presence of an NMR invisible intraerythrocytic sodium pool and assessment of the mechanisms explaining this invisibility was achieved by measurement of 23Na NMR signal intensities and T1 relaxation times of erythrocyte hemolysate during ion-competitive sodium release from association sites. Signal intensities after addition of small quantities of K+ and Mg2+ to the hemolysates were significantly larger than that expected from dilution of the sample, implying that the additions have resulted in the release of formerly invisible sodium. Furthermore, the intensities following the addition of K+ were significantly larger than those after the addition of Li+ and choline+. This signifies a specificity of the association sites at which sodium has decreased visibility. Increased T1 values following the additions confirmed the release of bound sodium.

Oral magnesium supplementation in patients with essential hypertension.

To elucidate the effects of magnesium on high blood pressure, a 4-week study of oral magnesium supplementation (MgO 1 g/day) was conducted in 21 outpatients with uncomplicated essential hypertension. During the study, blood pressure and intraerythrocyte sodium concentration decreased significantly, and the erythrocyte ouabain-sensitive 22Na efflux rate constant (Kos) and intraerythrocyte magnesium concentration both increased. Serum triglyceride and free fatty acid concentrations were reduced. Furthermore, the elevation in Kos significantly and positively correlated with both the increase in intraerythrocyte magnesium concentration and the decrease in mean blood pressure. There was a significant inverse correlation between the prestudy Kos and the decrease in mean blood pressure. In addition, when patients were divided according to their overall decrease in mean blood pressure, the prestudy intraerythrocyte sodium concentration was significantly higher in patients with a mean blood pressure decrease of more than 7 mm Hg than that of patients whose mean blood pressure decrease was less than 7 mm Hg. These results suggest that oral magnesium supplementation may lower blood pressure through the activation of a cell membrane sodium pump and may reduce serum lipid concentration. It also suggests that the lower the prestudy Kos or the higher the prestudy intraerythrocyte sodium concentration, the more effective the oral magnesium treatment is in lowering blood pressure. Therefore, we concluded that appropriate oral magnesium intake might be effective as a nonpharmacological treatment for essential hypertension.