Contraceptive progestins and gonadotropin secretion In vitro

Kiesel, L.; Helm, K.; Bertges, Karin; Maier, Christiane; Rabe, T.; Runnebaum, B.

doi:10.1016/0022-4731(87)90180-4

Cited by 6 publications

(1 citation statement)

References 36 publications

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“…Our understanding of the cellular mechanisms underlying progesterone (PI regulation of rat gonadotroph function in vitro has been derived primarily from studies on luteinizing hormone (LH) synthesis and secretion (Hsueh et al, 1979;Lagace et al, 1980;Tang, 1980;Drouin and Labrie, 1981;Turgeon and Waring, 1981Kiesel et al, 1987;Ortmann et al, 1989;Krey and Kamel, 1990a,b;. Only Labrie and his coworkers have examined the temporal characteristics of P modulation of follicle-stimulating hormone (FSH) by estrogen-treated gonadotrophs, noting that acute (< 6 h) and chronic (2 24 h) pretreatments increase the level of FSH secreted into the medium in response to gonadotropinreleasing hormone (GnRH; Drouin and Labrie, 1980;Lagace et al, 1980).…”

Section: Introductionmentioning

confidence: 99%

Progesterone modulation of gonadotropin secretion by dispersed rat pituitary cells in culture. IV. Follicle-stimulating hormone synthesis and release

Krey

Padmanabhan

Beitins

1993

Molecular and Cellular Endocrinology

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Estradiol-treated, rat pituitary cells were studied to examine the effects of progesterone (P) on follicle-stimulating hormone (FSH) synthesis and secretion. Progesterone was administered prior to or concurrent with 3 h secretory challenges with either gonadotropin-releasing hormone (GnRH), the iontophore A23187, the protein kinase C activator phorbol 12,13-myristate (PMA), or no secretagogue. Medium FSH levels and cell FSH stores were quantified by radioimmunoassay and bioassay. Acute (< 6 h) exposures to P increased medium levels of immunoreactive and bioactive FSH following GnRH challenge without influencing total (cell + medium) values whereas chronic (9-24 h) treatments increased both parameters. Chronic P elevated total FSH levels even when no secretagogue was present. Studies with antiprogestins, 5 alpha-dihydroprogesterone and 5 alpha-reductase inhibitors revealed that this direct action of P depended on progestin receptor occupation but not on 5 alpha-reduction. These studies indicate that P selectively increases bioactive and immunoactive FSH levels, presumably by increasing FSH synthesis, and characterize the time course and cellular mechanisms of this response. To accommodate for P modulation of total FSH levels, FSH secretion was standardized as the percentage of cellular stores available for release. Progesterone modulation of GnRH-stimulated FSH secretion was multiphasic, i.e. increased at 0-6 h, unchanged at 9 h and suppressed at 24 h. Acute and chronic exposures to P similarly modulated A23187-stimulated FSH release, whereas both P treatments increased PMA-stimulated FSH secretion. In these experiments P modulated luteinizing hormone secretion in parallel fashion, suggesting that common cellular mechanisms underlie peptidergic and steroidal regulation of the secretion of both gonadotropins.

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