Abstract |
OCT, a non-calcemic analogue of 1,25(OH)2D3 has been found to have a more potent activity than that of 1,25(OH)2D3 regarding cell differentiation and immunopotentiation activity, and to prolong the average life span of MRL/l mice. Recently, we found that OCT effectively suppressed the secretion and synthesis of PTH without inducing hypercalcemia. In primary cultures of bovine parathyroid cells, OCT was capable of suppressing PTH release in a dose-dependent manner. OCT was also active in vivo, and, like 1,25(OH)2D3, decreased the pre-pro(PTH) mRNA levels. In a group of rats with CRF, daily administration of OCT, 8 ng i.p. for 2 weeks returned PTH levels to normal without changes in serum calcium. Preliminary results in dogs with CRF indicated that after the administration of OCT 5 micrograms i.v., N-terminal PTH decreased by 76% without changes in Ca. In conclusion, OCT may provide a unique contribution to the treatment of secondary hyperparathyroidism.
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Authors | Y Nishii, J Abe, T Mori, A J Brown, A S Dusso, J Finch, S Lopez-Hilker, J Morrissey, E Slatopolsky |
Journal | Contributions to nephrology
(Contrib Nephrol)
Vol. 91
Pg. 123-8
( 1991)
ISSN: 0302-5144 [Print] Switzerland |
PMID | 1800003
(Publication Type: Journal Article, Review)
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Chemical References |
- Parathyroid Hormone
- Calcitriol
- maxacalcitol
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Topics |
- Animals
- Calcitriol
(analogs & derivatives, metabolism, pharmacology)
- Cells, Cultured
- Humans
- Parathyroid Hormone
(biosynthesis, metabolism)
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