Inhibin Concentrations in Ovarian and Jugular Venous Plasma and the Relationship of Inhibin with Follicle-Stimulating Hormone and Luteinizing Hormone during the Ovine Estrous Cycle*

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Abstract
A heterologous RIA for ovine inhibin was developed which was sufficiently sensitive and specific to describe the peripheral concentrations of immunoreactive inhibin (ilNH) during the estrous cycle of the ewe and to examine the effects of cautery of ovarian follicles on concentrations of ilNH in ovarian and jugular venous plasma. Parallel logit-log dose-response lines were observed among ovine follicular fluid, ewe plasma, and pure native ovine (31 kDa) and bovine (31 kDa) inhibin. ilNH could not be detected in ovariectomized ewe plasma, and there was no apparent cross-reactivity with a variety of structurally related and unrelated hormones and peptides, except a monomeric form of the a-subunit of INH. ilNH in follicular fluid was 104-fold higher than that in ovarian venous plasma, which was 3-fold higher than that in peripheral plasma. Cautery of the follicles resulted in a 35% reduction in ilNH and an 81% reduction in estrogen concentrations in the ovarian vein within 10 min. During the estrous cycle, ilNH and FSH were inversely related in samples taken over 30 h in the luteal phase (r = –0.69; P < 0.001) and in the pre- and postovulatory phases (r = –0.45; P < 0.001). iINH and LH were not related in the luteal phase, but were weakly positively correlated in the follicular phase (r = 0.31; P < 0.01). iINH and estrogen concentrations in the follicular phase were also weakly correlated (r = 0.30; P < 0.001). Furthermore, ilNH concentrations rose in the follicular phase and decreased within 3–6 h of the preovulatory surges of LH and FSH, reaching a nadir around the time of the second rise in FSH 24–48 h later. It is concluded that 1) large antral follicles are a major source of peripheral ilNH during the ovine estrous cycle; 2) ilNH levels increase in the follicular phase with the growth of the dominant follicle and may be inhibited by the preovulatory surge of gonadotropin; 3) the fall in inhibin after the LH surge may be responsible for the second rise in FSH; and 4) the inverse relationship between FSH and ilNH is consistent with the hypothesis that inhibin is involved in the feedback regulation of FSH. (Endocrinology126: 528–535,1990)