Ovarian and Circulating Inhibin Levels in Immature Female Rats Treated with Gonadotropin and after Castration*

Abstract
The effects of gonadotropin (FSH, LH, and PMSG) treatment and castration on ovarian and circulating levels of inhibin in immature female rats has been investigated. PMSG (20 IU) induced a progressive increase in the concentration of inhibin in both the ovaries and peripheral blood. The circulating levels of inhibin were significantly elevated 6 h after treatment and were associated with reduced levels of FSH. Similar inverse relationships between inhibin and FSH were also observed 24 h and 64 h after PMSG injection. Mean potencies of inhibin activity in the peripheral blood were 4.9, 58, and 452 U/ml at 6, 24, and 64 h, respectively, and were accompanied by similarly elevated levels in the ovary. In contrast to PMSGprimed rats, where a gradual rise in circulating inhibin levels was observed, ovine FSH (2 μg) treatment induced a prompt increase in inhibin within 6 h, reaching values of 16.7 U/ml and returning to baseline levels by 24 h. The prompt rise of inhibin in response to FSH was also dose related. In rats given saline or ovine LH (2 μg), there were no alterations in inhibin levels in the ovary or blood at any time after treatment. Bilateral ovariectomy of PMSG-primed rats significantly reduced circulating inhibin levels with half-times of 30 min and 3 h. FSH rose more slowly postcastration than in control animals and did not reach comparable values until 48 h after bilateral ovariectomy. In PMSG-primed rats that were unilaterally ovariectomized, circulating levels of inhibin fell initially, but rose again 3–8 h after unilateral ovariectomy. In conclusion, these data demonstrate that ovarian and circulating inhibin levels in immature female rats can be elevated by PMSG and FSH treatment. The rapid disappearance of inhibin after bilateral or unilateral ovariectomy indicates that ovaries are the primary source of inhibin secreted into blood. Furthermore, the inverse relationship between inhibin and FSH in peripheral blood supports the view that inhibin is involved in the feedback regulation of FSH.