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Endocrinology, doi:10.1210/endo-115-4-1476
Endocrinology Vol. 115, No. 4 1476-1483
Copyright © 1984 by the Endocrine Society.
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Calcium Transport in Perfused Duodena from Normal Chicks: Enhancement within Fourteen Minutes of Exposure to 1,25-Dihydroxyvitamin D3*

ILKA NEMERE{dagger}, YOSHIO YOSHIMOTO{ddagger} and ANTHONY W. NORMAN§

Department of Biochemistry, University of California Riverside, California 92521

Abstract

The effect of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3) on calcium transport was studied in vascularly perfused duodena of normal, vitamin D-replete chicks. Addition of 130 pM 1,25(OH)2D3 to the perfusate resulted in a significant increase in 45Ca transport from the lumen to the vascular effluent within 14 µn; the transport rate rose to 140% of levels in comparable preparations exposed for 40 min to vehicle. No effects of 1,25(OH)2D3 were noted on the back flux or transfer of 45Ca from the vascular effluent to the lumen. Vascular perfusion with 100 µM colchicine, an antimicrotubular agent, abolished the rapid lumen-to-vascular effluent effect of 1,25(OH)2D3 on 45Ca transport, relative to preparations exposed to the secosteroid and 100 µM lumicolchicine, (a light inactivated analog of colchicine). Colchicine did not, however, alter basal 45Ca transport rates. Addition of 130 pM 1,25(OH)2D3 to the lumenal compartment of normal chicks or vascular perfusion of duodena from vitamin D-deficient birds failed to increase 45Ca transport above control levels. Perfusion of duodena from normal chicks with 650 pM 1,25(OH)2D3 further increased calcium transport to 170% of levels observed in preparations treated with 130 pM steroid, and 210% of levels in controls. Although 15 nM vitamin D3 had no effect, in one series of experiments 125 nM 25-hydroxyvitamin D3 elicited vascular calcium levels that were 185% of controls at 40 min. These results suggest that 1,25(OH)2D3 can act in vitamin D-replete animals to produce rapid unidirectional calcium transport responses (through unknown mechanisms), as well as by interaction with intestinal nuclear receptors in D-deficient animals to promote induction of protein(s) that support long acting calcium transport responses. (Endocrinology 115: 1476–1483, 1981)

Footnotes

* This work was supported by USPHS Grants T32-AM-07310 and AM-09012-018. This is paper XLV in a series entitled "Studies on the Mode of Action of Calciferol;" the previous paper in this series is "Intestinal Brush Border Hydrolase Topography: Effects of Vitamin D3 and Filipin by Nemere, I., C. S. Dunlap, and A. W. Norman, 1983, Biochim. Biophys. Acta 729:35.

{dagger} Present address: Department of Biology, University of California, San Diego, La Jolla, CA 92093.

{ddagger} Visiting Professor from the 3rd Division of Internal Medicine, Kobe University School of Medicine, Kobe, Japan.

§ To whom correspondence and requests for reprints should be addressed.

Received November 15, 1983.




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