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Research Article Free access | 10.1172/JCI107610

Direct Inhibitory Effect of Hypercalcemia on Renal Actions of Parathyroid Hormone

Nama Beck, Harbans Singh, Sarah W. Reed, and Bernard B. Davis

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

Find articles by Beck, N. in: PubMed | Google Scholar

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

Find articles by Singh, H. in: PubMed | Google Scholar

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

Find articles by Reed, S. in: PubMed | Google Scholar

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

Find articles by Davis, B. in: PubMed | Google Scholar

Published March 1, 1974 - More info

Published in Volume 53, Issue 3 on March 1, 1974
J Clin Invest. 1974;53(3):717–725. https://doi.org/10.1172/JCI107610.
© 1974 The American Society for Clinical Investigation
Published March 1, 1974 - Version history
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Abstract

The effects of calcium on the renal actions of parathyroid hormone (PTH) were studied in vivo and in vitro. In parathyroidectomized rats, variable levels of blood calcium concentration were induced by intravenous infusion of calcium. The renal responses to the injected PTH, i.e. phosphate and cyclic AMP excretion, were compared in these animals. After PTH injection, the increases of both phosphate and cyclic AMP excretion were less in the calcium-infused animals than in the control group without calcium infusion. There was an inverse correlation between the renal responses to PTH and plasma calcium concentration of 4.2-13.5 mg/100 ml. But calcium had no effect on phosphate excretion induced by infusion of dibutyryl cyclic AMP. In the in vitro experiments, the increase of cyclic AMP concentration in response to PTH was less in renal cortical slices taken from the calcium-infused animals than in ones from the control group without calcium infusion. Calcium also inhibited the activation of renal cortical adenylate cyclase in response to PTH, but calcium had no effect on phosphodiesterase. The data indicate that calcium directly inhibits renal actions of PTH both in vivo and in vitro. Such inhibitory mechanism is probably at or before the step of PTH-dependent cyclic AMP generation in the kidney.

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