Follicular waves and concentrations of steroids and inhibin A in ovarian venous blood during the luteal phase of the oestrous cycle in ewes with an ovarian autotransplant

Abstract

The dynamics of ovarian follicular development and the pattern of pituitary and ovarian hormone concentration were investigated during the luteal phase in ewes with autotransplanted ovaries. The follicles were measured by ultrasound and samples of ovarian and jugular venous blood were collected at intervals of 12 h. Blood samples were collected before and after a GnRH challenge (250 ng GnRH, i.v.) to allow the determination of basal and LH-stimulated concentration of ovarian steroids. Throughout the luteal phase, large antral follicles developed in three waves, each of which was preceded by a rise in the concentration of FSH (P<0·05). The concentrations of oestradiol and androstenedione in the unstimulated and LH-stimulated samples were similar (P>0·05) during the first 3 days of the luteal phase but differed thereafter, with the LH-stimulated being significantly higher than the basal concentrations (P<0·05). In the first wave of follicular development the changes in follicular size were accompanied by an increase in the concentration of ovarian steroids and inhibin A. During the second follicular wave, although changes in follicle diameter were similar to the first wave (P>0·05), the basal concentration of ovarian steroids and inhibin A remained unchanged throughout the period of emergence and demise of the large follicles. These results confirm that the development of large antral follicles during the luteal phase of the sheep occurs in successive waves that are associated with fluctuations in FSH secretion. However, while the results strongly suggest that fluctuations in both inhibin A and oestradiol secretion control FSH during the first follicular wave, the cause of the FSH fluctuations associated with waves two and three is unclear. Final resolution of this issue may need to await the development of a specific assay for dimeric inhibin B.