Biol Reprod Keystone Symposia Conference on Frontiers in Reproductive Biology & Regulation of Fertility.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by JORDAN, A. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by JORDAN, A. W.
Agricola
Right arrow Articles by JORDAN, A. W.

Biology of Reproduction, Vol 25, 327-331, Copyright © 1981 by Society for the Study of Reproduction

Effects of Prostaglandin F2agr Treatment on LH and Dibutyryl Cyclic AMP-Stimulated Progesterone Secretion by Isolated Rat Luteal Cells

ALEXANDER W. JORDAN 1

1 Division of Drug Biology, Pharmaceutical Research and Testing, Food and Drug Administration, Washington, D.C. 20204


During prostaglandin F2agr (PGF2agr)-induced luteolysis in the rat, serum progesterone concentrations fall rapidly. This luteolytic effect of PGF2agr may be due to an inhibition of LH-stimulated adenylate cyclase activity. It is not clear, however, whether membrane events alone are responsible for this effect or if additional lesions exist in the steroid biosynthetic pathway. The addition of 1 µM PGF2agr to dispersed rat luteal cells significantly inhibited both LH- and dibutyryl cAMP (dbcAMP)-stimulated progesterone secretion. When administered in vivo, PGF2agr reduced serum progesterone concentrations within 30 min. Dispersed luteal cells from PGF2agr-treated rats produced significantly less progesterone in response to LH and dbcAMP than did cells from untreated rats. These data suggest that PGF2agr-induced inhibition of progesterone production occurs at a site beyond cAMP formation in the steroidogenic pathway. Furthermore, the ability of PGF2agr to inhibit dbcAMP-stimulated steroidogenesis more effectively in vivo than in vitro suggests that PGF2agr may be acting both directly and indirectly to inhibit luteal cell function in vivo.

Note:
ACKNOWLEDGMENTS I thank Sylvia Colson for her expert technical assistance. In addition, I am grateful to Dr. John Pike, The Upjohn Co., for the gift of PGF2agr, Dr. Gordon Niswender for the progesterone antiserum, and the National Pituitary Agency, NIAMDD, for the ovine LH-21 used in this study.

Submitted on December 30, 1980
Accepted on April 28, 1981




This article has been cited by other articles:


Home page
 Am. J. Physiol. Endocrinol. Metab.Home page
K. Minegishi, M. Tanaka, O. Nishimura, S. Tanigaki, K. Miyakoshi, H. Ishimoto, and Y. Yoshimura
Reactive oxygen species mediate leukocyte-endothelium interactions in prostaglandin F2alpha -induced luteolysis in rats
Am J Physiol Endocrinol Metab, December 1, 2002; 283(6): E1308 - E1315.
[Abstract] [Full Text] [PDF]

Home page
 EndocrinologyHome page
Z. Liu and D. M. Stocco
Heat Shock-Induced Inhibition of Acute Steroidogenesis in MA-10 Cells Is Associated with Inhibition of the Synthesis of the Steroidogenic Acute Regulatory Protein
Endocrinology, July 1, 1997; 138(7): 2722 - 2728.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1981 by the Society for the Study of Reproduction.