The involvement of ovarian factors in maintaining the pituitary glands of female rats in a state of low LH responsiveness to LHRH

in Journal of Endocrinology
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ABSTRACT

The effects of discontinuation and restoration of ovarian influences on the pituitary LH response to LHRH in vitro were investigated.

When female rat pituitary glands taken on day 2 of dioestrus were incubated with LHRH the release of LH was low during the first hour (lag phase response) and afterwards a progressive, protein synthesis-dependent increase took place (second phase response), this being the self-priming action of LHRH.

Short-term discontinuation (less than 1 day) of ovarian influences on the rat pituitary gland in vivo (ovariectomy) or in vitro (incubation in medium only) resulted in an increased LHRH-induced LH response during the lag phase.

The biphasic LH response or the self-priming action of LHRH disappeared completely after long-term discontinuation of ovarian influences on the pituitary gland, LH release being at its maximum from the start of the incubation. The biphasic response was reinstated when ovaries were implanted under the kidney capsules of ovariectomized rats. Auto-implantation of an ovary into the spleen immediately after bilateral ovariectomy did not, however, prevent the disappearance of the LHRH self-priming action. Ovarian activity responsible for the presence of the low LH response during the lag phase was thus effectively removed by the liver, but inhibin-like activity suppressing serum FSH levels remained present. Silicone elastomer implants (s.c.) containing oestradiol-17β, implanted for 4 weeks, did not reverse the loss of the biphasic LH response to LHRH.

It is concluded that liver-labile factors released by the ovaries keep the pituitary gland in a state of low responsiveness to LHRH. By giving a sufficiently high LHRH stimulus this inhibitory effect is neutralized and transition to a highly responsive state can be achieved. The ovarian factor(s) is not identical to inhibin or oestradiol-17β.

J. Endocr. (1987) 112, 265–273

 

      Society for Endocrinology

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