Effect of prostaglandin E<sub>1</sub> on certain renal actions of parathyroid hormone

Nama P. Beck; Frederick R. DeRubertis; Michael F. Michelis; Robert D. Fusco; James B. Field; Bernard B. Davis

doi:10.1172/JCI107047

¹Veterans Administration Hospital, Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15240

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¹Veterans Administration Hospital, Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15240

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¹Veterans Administration Hospital, Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15240

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¹Veterans Administration Hospital, Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15240

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¹Veterans Administration Hospital, Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15240

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¹Veterans Administration Hospital, Department of Medicine, School of Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania 15240

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Published in Volume 51, Issue 9 on September 1, 1972
J Clin Invest. 1972;51(9):2352–2358. https://doi.org/10.1172/JCI107047.
© 1972 The American Society for Clinical Investigation

Published September 1, 1972 - Version history

Parathyroid hormone increased basal adenyl cyclase activity and that increase was inhibited by prostaglandin E₁ (PGE₁). Tissue cyclic 3′,5′-adenosine monophosphate (cyclic AMP) concentrations were increased by parathyroid hormone and that increase was likewise inhibited by PGE₁. Both parathyroid hormone and dibutyryl cyclic AMP increased ³²P incorporation into renal cortical phospholipids. PGE₁ diminished the effect of parathyroid hormone but not dibutyryl cyclic AMP to influence that parameter. PGE₁ likewise modulated the effect of parathyroid hormone but not dibutyryl cyclic AMP to decrease fractional phosphate reabsorption by the renal tubule. It is suggested that PGE₁ inhibits the effect of parathyroid hormone by decreasing its effect on adenyl cyclase. Such interaction may be important in modulating the intracellular action of parathyroid hormone on kidney cortex.