This study evaluated the effects of magnesium supplementation on the development of hypertension in spontaneously hypertensive rats (SHR) and assesses the actions of magnesium on extracellular and intracellular Ca2+, Na+, and K+ status. Ten-week-old SHR (n = 72) and Wistar-Kyoto rats (WKY) (n = 60) were divided into four groups: WKY, Mg-WKY (WKY receiving 650 mg/L Mg(2+)supplementation), SHR, and Mg-SHR (SHR receiving Mg2+). Rats were studied for 17 weeks. Serum and erythrocyte Mg2+ and Ca2+ (measured by atomic absorption spectroscopy) and Na+ and K+ (measured by flame photometry) were determined every 3 or 4 weeks. From 13 weeks of age, blood pressure (BP) was significantly elevated in SHR compared with age-matched WKY. BP was reduced (P < .01) in SHR after 10 weeks of Mg2+ supplementation and at 27 weeks of age, BP in SHR was 218 (12 mm Hg v 184 +/- 9 mm Hg) in Mg-SHR. From 18 weeks of age, serum and intracellular Mg2+ levels were significantly lower (P < .05) and from 21 weeks of age, erythrocyte Ca2+ was significantly higher in SHR than in WKY. Mg2+ supplementation normalized intracellular Mg2+ and Ca2+ concentrations in SHR. BP was inversely correlated with erythrocyte Mg2+ (r = -0.74, P < .01) and positively correlated with erythrocyte Ca2+ (r = 0.78, P < .001). In conclusion, long-term Mg2+ supplementation significantly attenuates, but does not prevent, the development of hypertension in SHR. Furthermore, intracellular Mg2+ deficiency and Ca2+ overload in SHR are normalized by Mg2+ treatment.

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We report the largest series in which 12 out of 54 patients with primary malignant hypertension requiring dialysis recovered sufficient renal function to allow withdrawal of dialysis. The patients were divided into recovery (RC; n = 12) and non-recovery (N-RC; n = 42) groups. The two groups were compared for variables which might predict RC. They were also assessed for survival. Nine of the RC and 6 of the N-RC patients presented with acute oliguria (p = 0.01). The initial mean arterial pressure was significantly higher in the RC than the N-RC group (178 ± 17 vs. 160 ± 27 mm Hg; p = 0.03). Although not statistically significant, more females recovered (8 of 12 vs. 16 of 42; p < 0.1). More patients presenting with serum creatinine concentrations < 1,000 μmol/l (11 mg/dl) recovered (p = 0.09), while the presence of microangiopathic-haemolytic anaemia occurred more frequently in the RC (7 of 10) than in the N-RC (15 of 35) group (p = 0.16). Age, kidney size, and the presence of hypertensive retinopathy did not distinguish between the two groups. RC patients had a greater long-term survival (Mantel-Cox χ² = 4.48; p = 0.03). The renal function RC may be related to the type of dialysis provided (intermittent peritoneal dialysis) and to the use of modern potent peripheral vasodilator antihypertensive agents. Potential renal function RC should always be considered in patients being dialyzed for primary malignant hypertension.

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Alterations in intracellular cation metabolism have been implicated in the pathophysiology of essential hypertension. Total magnesium, calcium, sodium and potassium levels were studied in serum erythrocytes and platelets, from 154 subjects (76 hypertensive and 78 normotensives; 104 blacks and 50 whites). In the combined black and white hypertensive group, platelet sodium and calcium and erythrocyte calcium were elevated and serum potassium, serum magnesium and platelet magnesium decreased. In the black hypertensive patients, platelet sodium and calcium and erythrocyte calcium were increased, whereas serum magnesium, serum potassium, platelet magnesium and erythrocyte magnesium were decreased. In the white hypertensive group, platelet sodium and erythrocyte calcium were raised and platelet magnesium was decreased. In the black hypertensive patients, serum and platelet magnesium and serum calcium were negatively and erythrocyte and platelet calcium positively correlated with mean arterial pressure. In the white hypertensive patients platelet sodium was directly related to mean arterial pressure. These results suggest that intracellular sodium and calcium overload and magnesium depletion may be important in the pathophysiology of hypertension. Magnesium disturbances are more consistent and widespread in black hypertensive patients than in white hypertensive patients.