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Kinetics of Erythrocyte Plasma Membrane (Ca²⁺,Mg²⁺)ATPase in Familial Benign Hypercalcemia^*

Endocrine Research Unit, Division of Endocrinology and Metabolism, Department of Medicine (H.J.D., H.H.), and the Department of Molecular Biology and Biochemistry (J.T.P.), Mayo Clinic and Foundation, Mayo Medical School Rochester, Minnesota 55905

Address requests for reprints to: Dr. Henry J. Donahue, Musculo-Skeletal Research Laboratory, Department of Orthopedics, Health Sciences Center, State University of New York, Stony Brook, NY 11794.

The pathogenesis of familial benign hypercalcemia (FBH) is unknown. Possible explanations for the disorder include a set-point error in parathyroid gland regulation and intrinsic renal hyperreabsorption of calcium. Thus, FBH may involve an alteration in cellular calcium transport, especially in renal and parathyroid cells. A primary mediator of cellular calcium transport is (Ca²⁺,Mg²⁺)ATPase. Therefore, we examined in detail the kinetics of (Ca²⁺,Mg²⁺)ATPase activity in erythrocyte plasma membranes from 11 patients with FBH from 7 families, 5 patients with untreated primary hyperparathyroidism, and equal numbers of age- and sex-matched normal subjects. (Ca²⁺,Mg²⁺)ATPase activity was measured in isolated membranes as a function of free calcium (0.05–300 µmol/L) in the presence or absence of calmodulin (600 nmol/L) and as a function of calmodulin (0–1800 nmol/L). We found no significant differences in calcium- or calmodulin-dependent (Ca²⁺,Mg²⁺)ATPase kinetics between patients with FBH or primary hyperparathyroidism and their age- and sex-matched normal subjects. None of the kinetic parameters was correlated with serum calcium or serum PTH values. We postulate that a mechanism other than a global defect in (Ca²⁺Mg²⁺)ATPase activity is responsible for the hypercalcemia in patients with FBH.

^* This work was supported in part by grants from the USPHS, NIH, Bethesda, MD (AR-32526, DK-38855, and RR-585). Portions of this work were presented at the National Meetings of the American Society for Bone and Mineral Research, Indianapolis, IN, 1987, and New Orleans, LA, 1988.

Received October 17, 1988.

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