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Research Article Free access | 10.1172/JCI105648
Department of Pharmacology, University of Rochester School of Medicine and Dentistry, Rochester, New York
Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York
‡Burroughs Wellcome Scholar in Clinical Pharmacology.
Address requests for reprints to Dr. William Y. W. Au, Departments of Pharmacology and Medicine, University of Rochester, School of Medicine and Dentistry, Rochester, N. Y. 14620.
*Received for publication 31 March 1967 and in revised form 15 June 1967.
This study was supported by Grant AM 07871 from the U. S. Public Health Service.
A preliminary report of this work has been published in abstract form (1).
Find articles by Au, W. in: JCI | PubMed | Google Scholar
Department of Pharmacology, University of Rochester School of Medicine and Dentistry, Rochester, New York
Department of Medicine, University of Rochester School of Medicine and Dentistry, Rochester, New York
‡Burroughs Wellcome Scholar in Clinical Pharmacology.
Address requests for reprints to Dr. William Y. W. Au, Departments of Pharmacology and Medicine, University of Rochester, School of Medicine and Dentistry, Rochester, N. Y. 14620.
*Received for publication 31 March 1967 and in revised form 15 June 1967.
This study was supported by Grant AM 07871 from the U. S. Public Health Service.
A preliminary report of this work has been published in abstract form (1).
Find articles by Raisz, L. in: JCI | PubMed | Google Scholar
Published October 1, 1967 - More info
The effects of treatment with vitamin D, calcium, or lactose on the responsiveness of vitamin D—deficient rats to parathyroid hormone were compared. In the absence of vitamin D, parenteral calcium or dietary lactose administration resulted in increases in serum calcium concentration although not to the normal values obtained in animals given vitamin D. Dietary lactose also partially restored the low bone calcium content of vitamin D—deficient rats. Untreated vitamin D—deficient rats showed no significant changes in serum calcium concentration after parathyroidectomy or parathyroid extract administration. Vitamin D, lactose, and calcium all restored responsiveness to parathyroid hormone; serum calcium concentration decreased after parathyroidectomy and showed a dose-related increase in response to parathyroid extract. Hence, the unresponsiveness to parathyroid hormone in vitamin D deficiency may be due to a lack of calcium at a local site of action, presumably bone, rather than to the absence of vitamin D as a specific cofactor.