The effect of ovarian arterial infusion of human recombinant inhibin and bovine follicular fluid on ovarian hormone secretion by ewes with an autotransplanted ovary.
Recombinant human inhibin A (rhInh) or steroid-free bovine follicular fluid (bFF) were infused into the ovarian artery of anoestrous ewes with ovarian autotransplants induced to ovulate with a pulsatile regimen of GnRH applied after a 10-day pretreatment with progestagen sponges. In the period 12-24 h after sponge withdrawal ewes received ovarian arterial infusions of saline (n = 6), 0.3 micrograms rhInh/h (n = 5), 1.6 micrograms rhInh/h (n = 5) or 25 microliters bFF/h (n = 4). Controls had a normal follicular phase with an LH surge 43 +/- 3 h after sponge withdrawal which resulted in ovulation (six out of six). Both doses of rhInh increased ovarian venous inhibin concentrations in a dose-related fashion (P < 0.05) but resulted in depressions (P < 0.05) in FSH concentrations of similar magnitude. Both doses of rhInh acutely inhibited ovarian oestradiol and androstenedione secretion (P < 0.01) but at the end of rhInh infusion oestradiol secretion was quickly re-established without a corresponding increase in FSH. LH surges were detected in five out of five and three out of five ewes infused with low and high doses of rhInh respectively, and progesterone concentrations during the subsequent luteal phase were depressed (P < 0.05). Infusion of bFF had no effect on inhibin or FSH concentrations but resulted in acute inhibition (P < 0.01) of ovarian oestradiol, androstenedione and inhibin secretion, a delay (P < 0.05) in the time to the LH surge and a depression (P < 0.05) in luteal-phase progesterone concentrations. In conclusion, while the depression in FSH induced by rhInh cannot be excluded as a cause for the inhibitory effects of rhInh treatment on ovarian function, such a mechanism cannot fully explain the ovarian responses obtained to rhInh infusion. These results therefore support a direct ovarian role for inhibin in the modulation of ovarian function in addition to its indirect role in controlling FSH. This conclusion is supported by the demonstration that bFF can induce similar inhibitory effects on ovarian function without changing FSH.
Campbell
B K
BK
CSIRO Division of Animal Production, Blacktown, New South Wales, Australia.
Scaramuzzi
R J
RJ
D000735:Androstenedione / Q000378:metabolism; D000818:Animals; D002417:Cattle; D003864:Depression, Chemical; D004958:Estradiol / Q000378:metabolism; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism; D015571:Follicular Fluid / Q000378:metabolism*; D012739:Gonadal Steroid Hormones / Q000378:metabolism*; D007987:Gonadotropin-Releasing Hormone / Q000494:pharmacology; D006801:Humans; D007261:Infusions, Intra-Arterial; D007265:Inhibins / Q000008:administration & dosage / Q000378:metabolism / Q000494:pharmacology*; D007986:Luteinizing Hormone / Q000378:metabolism; D008954:Models, Biological; D010053:Ovary / Q000098:blood supply / Q000378:metabolism* / Q000637:transplantation; D011374:Progesterone / Q000097:blood; D011994:Recombinant Proteins / Q000494:pharmacology; D012756:Sheep; D014182:Transplantation, Autologous
D012739:Gonadal Steroid Hormones; D011994:Recombinant Proteins; D007987:Gonadotropin-Releasing Hormone; D000735:Androstenedione; D011374:Progesterone; D004958:Estradiol; D007265:Inhibins; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone