Effect of estrogen on adenosine 3'5',cyclic monophosphate in quail oviduct: possible involvement in estradiol-activated growth.
Previous studies have shown that estradiol indirectly stimulated the proliferation of oviduct epithelial cells in the quail. The present study was undertaken to investigate the effects of estradiol and other steroid hormones on the cAMP concentration. The ability of forskolin, a specific activator of the catalytic subunit of adenylate cyclase, to induce oviduct cell proliferation and specific protein synthesis (progesterone receptor) in the absence of estrogen was also tested. Administration of estradiol benzoate (EB) to immature female quails produced a transient surge in oviduct cAMP concentration. After EB injection, cAMP concentration increased by 36.7% after 6 h and returned to control values after 12 h. This rise in oviduct cAMP concentration preceded the beginning of DNA synthesis. The same effect was observed even in the absence of increased plasma estradiol, when the hormone was perfused through the hepatic portal vein. Estriol, estrone, and testosterone failed to elevate cAMP concentrations. After repeated EB injections, the oviduct cAMP concentration declined below the control value (-66% after 72 h). A similar drop in the cAMP concentration was observed in developing quails during the proliferative phase of the luminal epithelial and glandular cells. Administration of forskolin to immature female quail pretreated with EB rapidly increased the oviduct cAMP concentration, induced a burst of DNA synthesis, and shortened the prereplicative period. In addition, forskolin administration did not increase the progesterone receptor concentration. These results demonstrate that cAMP is involved in the mechanism by which estradiol indirectly stimulates oviduct epithelial cell proliferation in the quail. The events that may take place during the prereplicative period and the antiproliferative effect of progesterone through a sustained increase in the cAMP concentration in the oviduct are discussed.
Laugier
C
C
Laboratoire de Physiologie Pharmacodynamie, Institut National des Sciences Appliquées, Villeurbanne, France.
Courion
C
C
Pageaux
J F
JF
Fanidi
A
A
Dumas
M Y
MY
Sandoz
D
D
Nemoz
G
G
Prigent
A F
AF
Pacheco
H
H
D000818:Animals; D002455:Cell Division / Q000187:drug effects; D005576:Colforsin / Q000494:pharmacology; D003370:Coturnix; D000242:Cyclic AMP / Q000378:metabolism*; D004261:DNA Replication / Q000187:drug effects; D004958:Estradiol / Q000494:pharmacology; D004964:Estriol / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D004970:Estrone / Q000494:pharmacology; D005260:Female; D007700:Kinetics; D009929:Organ Size / Q000187:drug effects; D010057:Oviducts / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D011980:Receptors, Progesterone / Q000378:metabolism
D004967:Estrogens; D011980:Receptors, Progesterone; D005576:Colforsin; D004970:Estrone; D004958:Estradiol; D000242:Cyclic AMP; D004964:Estriol