Disturbances of renal and erythrocyte calcium handling in rats of the Milan hypertensive strain.

Urinary calcium (Ca) excretion and erythrocyte membrane Ca binding and transport were investigated in rats of the Milan hypertensive (MHS) and normotensive strains (MNS). Despite slightly reduced ionized Ca levels in the serum, MHS significantly increased urinary Ca excretion under fasting conditions (P less than 0.01). Urinary Ca was positively related to sodium (Na) excretion in both rat strains; moreover the urinary Ca:Na ratio was significantly enhanced in MHS rats (P less than 0.05). These data suggest that in MHS, Ca reabsorption in the renal tubular cell is reduced independently of disturbances in Na handling. Adenosine triphosphate (ATP)-dependent Ca transport, reflecting the Ca, magnesium (Mg)-ATPase activity (Ca pump), was measured in inside-out vesicles obtained from erythrocyte membranes. This variable was significantly reduced in MHS (P less than 0.01), with no change in the Ca pump affinity constant for Ca. Calcium binding to erythrocyte membranes, measured in the presence of free Ca concentrations comparable with those of the intracellular fluid, was found to be significantly reduced (P less than 0.01) in MHS rats because of the lower number of Ca binding sites. These abnormalities of red blood cell (RBC) Ca handling are in keeping with the increased Ca clearance observed in the kidney. It is not clear whether the disturbances of renal and erythrocyte Ca handling were a genetic primary defect or a secondary change of membrane function.