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Research Article Free access | 10.1172/JCI106746

Effects of vasopressin and prostaglandin E1 on the adenyl cyclase—cyclic 3′,5′-adenosine monophosphate system of the renal medulla of the rat

Nama P. Beck, Toshio Kaneko, Uriel Zor, James B. Field, and Bernard B. Davis

1Department of Medicine, The Oakland Veterans Administration Hospital, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

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

1Department of Medicine, The Oakland Veterans Administration Hospital, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

Find articles by Kaneko, T. in: JCI | PubMed | Google Scholar

1Department of Medicine, The Oakland Veterans Administration Hospital, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

Find articles by Zor, U. in: JCI | PubMed | Google Scholar

1Department of Medicine, The Oakland Veterans Administration Hospital, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

Find articles by Field, J. in: JCI | PubMed | Google Scholar

1Department of Medicine, The Oakland Veterans Administration Hospital, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15213

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

Published December 1, 1971 - More info

Published in Volume 50, Issue 12 on December 1, 1971
J Clin Invest. 1971;50(12):2461–2465. https://doi.org/10.1172/JCI106746.
© 1971 The American Society for Clinical Investigation
Published December 1, 1971 - Version history
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Abstract

Vasopressin increased adenyl cyclase activity in homogenates of both inner and outer renal medulla of the rat. It also increased the concentration of cyclic 3′,5′-adenosine monophosphate (AMP) in slices of both inner and outer medulla but not in renal cortex. In the inner medulla, a concentration of prostaglandin E1 (PGE1), which was ineffective by itself significantly reduced the stimulation of adenyl cyclase activity and cyclic AMP concentration induced by vasopressin. These results are consistent with the hypothesis that PGE1 can compete with vasopressin for adenyl cyclase-binding sites. However, the findings in the outer medulla suggest the situation is more complex. Although 10-8 M PGE1 had no effect by itself and inhibited the vasopressin-induced elevation of cyclic AMP, larger amounts of PGE1 increased both adenyl cyclase activity and cyclic AMP levels. The maximum effect on the latter parameter was at least 6 times as great as that of maximum amounts of vasopressin.

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