title: Formation of cyclic adenosine monophosphate (cAMP) in the preovulatory rabbit follicle: role of prostaglandins and steroids.
abstract: The preovulatory increase in follicular prostaglandins (PG) stimulated by luteinizing hormone (LH) is dependent upon 3'-5'-cyclic adenosine monophosphate (cAMP) and is essential for ovulation. It has been proposed that follicular PG stimulate a second rise in cAMP, independent of LH. This study examined the temporal relationships among PGE2, PGF2 alpha 6-keto-PGF1 alpha, estradiol-17 beta, progesterone, testosterone, androstenedione and the biphasic increases of cAMP in follicles of rabbits. Does received indomethacin (IN, 20 mg/kg, i.v.; n = 30) or phosphate buffer (C; n = 30), 0.5 h before 50 ug of LH. At laparotomy at 0, 0.5, 1, 2, 4 or 8 h after LH, blood was collected from each ovarian vein and two follicles per ovary were aspirated of fluid and excised. Plasma and follicular tissue and fluid were assayed for PG and steroids. Tissue and fluid were assayed for cAMP. In C does, cAMP (pmol/follicle) in tissue increased from 11.3 at 0 h to 14.2 at 0.5 h, decreased at 1 h (5.4) and increased linearly through 8 h to 14.5. In IN-treated does, cAMP remained high from 0.5 (13.2) to 2 h (16.3), decreased at 4 h (7.9) then increased again by 8 h (15.5). Indomethacin decreased all PG in follicular tissue but 6-keto-PGF1 alpha rose after 2 h, whereas PGE2 and PGF2 alpha did not. Estradiol-17 beta, progesterone, and androstenedione did not vary with treatment; testosterone was increased (P less than .05) by IN. PGE2 or PGF2 alpha may terminate the first phase of cAMP production, rather than initiate the second phase.
authors.forename: R C
authors.initials: RC
authors.lastname: Rhodes
authors.forename: M W
authors.initials: MW
authors.lastname: Fleming
authors.forename: W J
authors.initials: WJ
authors.lastname: Murdoch
authors.forename: E K
authors.initials: EK
authors.lastname: Inskeep
mesh_terms: D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000735:Androstenedione / Q000378:metabolism; D000818:Animals; D000242:Cyclic AMP / Q000096:biosynthesis*; D015237:Dinoprost; D015232:Dinoprostone; D011464:Epoprostenol / Q000096:biosynthesis; D005260:Female; D007213:Indomethacin / Q000494:pharmacology; D007986:Luteinizing Hormone / Q000494:pharmacology; D006080:Ovarian Follicle / Q000378:metabolism*; D010060:Ovulation / Q000187:drug effects; D011374:Progesterone / Q000378:metabolism; D011453:Prostaglandins / Q000378:metabolism*; D011458:Prostaglandins E / Q000032:analysis; D011460:Prostaglandins F / Q000032:analysis; D011817:Rabbits; D013739:Testosterone / Q000378:metabolism
chemical_list: D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D013739:Testosterone; D000735:Androstenedione; D011374:Progesterone; D015121:6-Ketoprostaglandin F1 alpha; D007986:Luteinizing Hormone; D015237:Dinoprost; D011464:Epoprostenol; D000242:Cyclic AMP; D015232:Dinoprostone; D007213:Indomethacin