Active immunization of sheep against androstenedione results in an increase in ovulation rate that is associated with increased plasma levels of LH and progesterone, but not FSH. Although immunized ewes have more activated follicles the secretion rate of oestradiol is not increased. An experiment was conducted to examine the effect of androstenedione immunity on the ovarian secretion and peripheral plasma concentrations of inhibin.
Merino ewes in which the left ovary had been autotransplanted to a site in the neck were divided into control (n = 5) and androstenedione-immune (n = 6) groups. Ovarian and jugular venous blood was collected every 10 min at two stages of the follicular phase, 21–27 h and 38–42 h after a luteolytic dose of an analogue of prostaglandin F2α (PG), and every 15 min for 6 h on day 10 of the subsequent luteal phase. The ewes were monitored regularly for luteal function by measurement of the concentration of progesterone and preovulatory LH surges. The concentration of inhibin in jugular and ovarian venous plasma was determined by radioimmunoassay and ovarian secretion rates and peripheral concentrations are expressed as pg of 1–26 peptide fragment of the α chain.
The ovarian secretion rate of inhibin tended to be greater in androstenedione-immune ewes at all stages of the oestrous cycle measured, with this difference being statistically significant (P <0·05) during the luteal phase (100±40 and 260±80 (s.e.m.) pg/min for control and immune groups respectively). The pattern of ovarian inhibin secretion exhibited pulsatile-like fluctuations which were not associated with LH pulses. Peripheral concentrations of inhibin were generally higher in immunized than in control ewes with this difference being significant (P < 0·01) from day 4 to 14 of the luteal phase (59±5 and 110±7 ng/1 for control and immune respectively). The ovarian secretion rate of immunoactive inhibin was greater (P <0·01) during the follicular phase than during the luteal phase in both groups of ewes, and peripheral concentrations of inhibin increased (P < 0·001) following injection of PG in ewes from both treatment groups.
We concluded that androstenedione immunity results in an increase in ovarian inhibin secretion, an effect that can probably be attributed to the greater number of large oestrogenic follicles present in the ovaries of these ewes. Furthermore, this increase in the concentration of inhibin may override any decrease in the negative feedback effects of ovarian steroid produced by immunization and, hence, explain the paradoxical findings of normal concentrations of FSH and raised concentrations of LH in ewes which are immunized against androstenedione.
Journal of Endocrinology (1990) 127, 285–296
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