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Department of Oral Biology, University of Connecticut Health Center (G.A.R., S.B.R.) Farmington, I Connecticut 06032
The Department of Anatomy, Medical Center, University of Massachusetts (S.C.M.) Worcester, Massachusetts 01605
Requests for reprints and correspondence should be addressed to: Dr. G. A. Rodan, Department of Oral Biology, University of Connecticut Health Center, Farmington, Connecticut 06032.
Abstract
We have examined the effect of parathyroid hormone (PTH) on the adenylate cyclase activity of newborn osteopetrotic rat calvaria, to study a possible molecular basis for the reduced response of this mutant to PTH. Phenotypically normal littermates served as controls. We also measured the effect of PTH on kidney adenylate cyclase activity and on lactic acid accumulation in short term cultures of calvaria. PTH stimulated calvarial adenylate cyclase activity in a dose-dependent manner in both mutant rats and normal littermates. Lactic acid production was also enhanced by PTH, and no significant difference between mutants and normal littermates was observed. These findings indicate that the reduced response of the young osteopetrotic rats to PTH is not due to an absence of PTH receptors coupled to adenylate cyclase. (Endocrinology 102: 1501, 1978)
Footnotes
* This work was supported by NIH Research Grants AM-17848 and DE-03818.
Received May 18, 1977.
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