Influence of Sodium and Parathyroid Hormone on Calcium Release from Intestinal Mucosal Cells

Stanley J. Birge; Sandra C. Switzer; David R. Leonard

doi:10.1172/JCI107808

^{Department of Medicine, The Jewish Hospital of St. Louis, St. Louis, Missouri 63110}

^{Department of Washington University School of Medicine, St. Louis, Missouri 63110}

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^{Department of Medicine, The Jewish Hospital of St. Louis, St. Louis, Missouri 63110}

^{Department of Washington University School of Medicine, St. Louis, Missouri 63110}

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^{Department of Medicine, The Jewish Hospital of St. Louis, St. Louis, Missouri 63110}

^{Department of Washington University School of Medicine, St. Louis, Missouri 63110}

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Published in Volume 54, Issue 3 on September 1, 1974
J Clin Invest. 1974;54(3):702–709. https://doi.org/10.1172/JCI107808.
© 1974 The American Society for Clinical Investigation

Published September 1, 1974 - Version history

The uptake and release of ⁴⁵Ca from the intestinal mucosal epithelium were investigated under a variety of conditions. The initial rate of uptake characterized a calcium pool with a half-time of saturation of less than 2 min. The entry of ⁴⁵Ca into this pool was inhibited by NaCN and ethacrynic acid and was stimulated by the removal of Cl^- from the incubation. The initial rate of ⁴⁵Ca release was also inhibited by NaCN and removal of Na⁺ from the incubation. Parathyroid hormone administration enhanced the release of ⁴⁵Ca from cells prepared from parathyroid-ectomized animals. These observations suggest that calcium transport across the brush border and basallateral membranes are identifiable components of the kinetics of ⁴⁵Ca uptake and release and that parathyroid hormone stimulates a sodium-dependent mechanism of calcium transport across the basal-lateral membranes.