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Effects of Hyperthyroidism and Hypothyroidism on Human Red Blood Cell Ca²⁺-ATPase Activity^*

Endocrinology Division, Department of Medicine, State University of New York at Buffalo School of Medicine, Veterans Administration Medical Center Buffalo, New York 14215

Address all correspondence and requests for reprints to: Paul J. Davis, M.D., Erie County Medical Center, 462 Grider Street, Buffalo, New York 14215.

Erythrocyte Ca²⁺-ATPase activity was measured in membrane ghosts from hyperthyroid and hypothyroid patients and compared with that in normal subjects. Basal enzyme activity was significantly increased in the hyperthyroid group and decreased in the hypothyroid group. In vitro responsiveness of the enzyme to calmodulin, the activator protein for Ca²⁺- TPase, and to T₄ was decreased in both hyper- and hypothyroid ghosts. Although the membrane content of endogenous calmodulin was low in hypothyroidism, this is an unlikely explanation for the low basal activity of Ca²⁺-ATPase.

A limited number of patients from each group were restudied when they were euthyroid after 8 or more months of treatment. Basal, T₄-stimulated, and calmodulin-stimulated Ca²⁺-ATPase activities returned to normal, with the exception of calmodulin responsiveness in the membranes from previously hypothyroid patients. This decreased responsiveness may have been a reflection of either increased patient age or underlying chronic (nonthyroidal) illness.

This study provides clinical confirmation of previously reported in vitro studies suggesting that the set-point of Ca²⁺- ATPase activity is, in part, a function of endogenous thyroid hormone levels.

^* This work was supported by V.A. Merit Review research funds.

Received May 20, 1985.