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Endocrinology, doi:10.1210/endo-101-3-876
Endocrinology Vol. 101, No. 3 876-882
Copyright © 1977 by the Endocrine Society.
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Modulation of Ovarian Adenylate Cyclase Response to Gonadotropins Following Luteinization of the Rat Ovary

C. Y. LEE*

Department of Laboratory Medicine and Pathology, University of Minnesota Minneapolis, Minnesota, 55455 Department of Molecular Medicine, Mayo Clinic and Mayo Foundation Rochester, Minnesota 55901

Abstract

The hFSH- and hLH-sensitive adenylate cyclase activities of immature and luteinized rat ovaries were studied. Both immature and luteinized ovaries contain an enzyme activity highly responsive to gonadotropin stimulation. Satisfactory response of the ovarian adenylate cyclase activity obtained under optimal conditions required gentle homogenization of ovarian tissues. The enzyme activity of the immature ovaries was highly sensitive to hFSH (5- to 7-fold over the basal activity). The stimulation cannot be attributed to hLH contamination, since hFSH had a larger stimulatory effect than hLH in immature ovaries and the apparent Km for both hFSH and hLH were about the same. The adenylate cyclase of the heavily luteinized ovaries was found more responsive to hLH after luteinization by PMSG-hCG injection. hLH caused an average 6-fold increase in enzyme activity. On the other hand, the adenylate cyclase of the luteinized ovaries lost its response to FSH. The hFSH-stimulated activity observed could be attributed to hLH contamination, since the apparent Km for hFSH was markedly higher (92 to 102 x 10M–9M) than that for hLH (6.1 x 10–9M). The loss of FSH-stimulated adenylate cyclase activity associated with the increase in LH-stimulated activity of the luteinized ovaries is consistent with the previous findings of disappearance of FSH receptors and increase in LH receptors following luteinization. These data indicate that modulation of the gonadotropin receptoradenylate cyclase system can be important in the regulation of ovarian response to gonadotropin stimulation.

Footnotes

Supported by grants from USPHS (HD 10075 and HD 9140).

Part of this work was presented at the 58th Annual Meeting of the Endocrine Society, San Francisco, California, June 23–25, 1976.

* Present address: Department of Laboratory Medicine and Pathology, University of Minnesota, Minneapolis, Minnesota 55455.

Received August 25, 1976.







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Copyright © 1977 by The Endocrine Society