Na+/Mg2+ antiport in erythrocytes of spontaneously hypertensive rats: role of Mg2+ in the pathogenesis of hypertension.

Total Mg2+ content in plasma and erythrocytes did not significantly differ between WKY and SHR. Mg2+ efflux via Na+/Mg2+ antiport was 10% lower in non Mg(2+)-loaded erythrocytes of SHR than in WKY, and 16% lower in Mg(2+)-loaded erythrocytes of SHR. The activation of Na+/Mg2+ antiport in erythrocytes by Cl-, as tested by substitution of Cl- with SCN-, and the regulation of Na+/Mg2+ antiport by protein kinases, as tested by PMA and staurosporine, showed no differences between WKY and SHR. The reduction of Na+/Mg2+ antiport was explained by a reduction in the number of Na+/Mg2+ antiporter molecules in SHR erythrocytes. Mg2+ efflux in KCl medium by K+/Mg2+ antiport via the unspecific choline exchanger was not significantly reduced in SHR and was equally affected by PMA and staurosporine in WKY and SHR. An explanation for some controversial results, unchanged or reduced concentration of Mg2+ in serum, total Mg2+ and free Mg2+ in erythrocytes of SHR and patients with essential hypertension was proposed. The role of Na+/Mg2+ antiport and [Mg2+]i in the pathogenesis of experimental and clinical hypertension was discussed.