Abstract:
:Angiotensin II (AII) is present in the mammalian ovary and has been correlated with atresia in follicles. Since the theca interna may be one site at which atresia is initiated, we wished to determine whether AII exerts an effect on theca interna from explanted ovarian follicles of hamsters. Hamsters were sacrified on the morning of proestrus, and ovaries were removed. Preovulatory follicles were excised from the ovaries, and cultured with one of the following components: medium alone (control); medium plus AII (1 x 10(-6) M); the AII-receptor antagonist [Sar1, Ile8] AII (1 x 10(-4) M); or AII plus antagonist. After 72 h, the follicles were processed for transmission electron microscopy (to determine quantities of theca interna organelles involved in the steroid synthetic pathway) or for protein determination (to normalize steroid production rates). The incubation medium was drawn off and analyzed by radioimmunoassay for progesterone, androstenedione, or estradiol-17 beta. There was a significant positive correlation (r = 0.92, P less than 0.01) between follicular androstenedione secretion and area comprising theca interna smooth endoplasmic reticulum. In the theca interna, AII induced a two-fold and 1.6-fold increase in lipid droplet number and area comprising smooth endoplasmic reticulum, respectively (P less than 0.05). Excess antagonist negated the increase in cell organelles and also reduced androstenedione secretion compared with AII alone (P less than 0.05). Most importantly, AII significantly augmented the ratio of androstenedione:estradiol-17 beta secretion by 44% over that of control. The ultrastructural changes observed in this study and the increase in the androstenedione:estradiol-17 beta production ratio are consistent with atresia-like changes in ovarian follicles.(ABSTRACT TRUNCATED AT 250 WORDS)
journal_name
Cell Tissue Resjournal_title
Cell and tissue researchauthors
Kitzman PH,Hutz RJdoi
10.1007/BF00338068keywords:
subject
Has Abstractpub_date
1992-04-01 00:00:00pages
191-6issue
1eissn
0302-766Xissn
1432-0878journal_volume
268pub_type
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