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Molecular Pharmacology, Vol 16, 932-940, Copyright © 1979 by the American Society for Pharmacology and Experimental Therapeutics
1 Department of Pharmacology and Therapeutics, Texas Tech University School of Medicine,
Lubbock, Texas 79430
In vivo administration of estradiol benzoate (E2B) or parathyroid hormone (PTH) stimulates in vitro renal conversion of 25-hydroxyvitamin D3 [25-(OH)D3] to 1,25-dihydroxyvitamin D3 [1,25-(OH)2D3] in birds. In the present investigation, the effect of PTH on 1,25-(OH)2D3 production was studied in female Japanese quail pretreated with the antiestrogen, tamoxifen citrate (30 mg/kg) daily for 7 days. PTH was injected at two different doses (92 and 275 U.S.P. units/kg) every 8 hours during the last two days of tamoxifen treatment. E2B (0.1 and 1.0 mg/kg) was injected 24 hours before sacrifice. Control groups received vehicle only. All injections were given intramuscularly. Kidney homogenates were prepared and incubated with tritiated 25-(OH)D3. E2B-induced stimulation of 1,25-(OH)2D3 production was completely blocked by prior treatment with tamoxifen, but PTH-induced stimulation of 1,25-(OH)2D3 production was unaffected by antiestrogen treatment. When PTH and E2B were injected together, no additive effects on either 1,25-(OH)2D3 production or hypercalcemia were observed. The data indicate that estrogen receptors are not an essential link in the chain of events mediating the PTH-induced stimulation of 1,25-(OH)2D3 production.
Note:
ACKNOWLEDGMENTS
The authors are grateful for the technical assistance
of Stephen M. Fuller, Vicki D. Edgington and Ingrid
L. Greene.