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Prolactin, Growth Hormone, and Luteinizing Hormone in the Maintenance of Testicular Luteinizing Hormone Receptors^*

WILLIAM B. ZIPF, ANITA H. PAYNE and ROBERT P. KELCH

Departments of Obstetrics and Gynecology, Biological Chemistry, and Pediatrics, University of Michigan Ann Arbor, Michigan 48109

Address requests for reprints to: A. H. Payne, Department of Obstetrics and Gynecology, University of Michigan, Ann Arbor, Michigan 48109.

Abstract

To elucidate further pituitary influence on testicular function, we studied the effect of PRL, GH, and LH alone or in various combinations on the maintenance of testicular LH receptor concentration and testosterone synthesis in response to LH (testicular responsiveness) in hypophysectomized adult rats. Hypophysectomy reduced LH receptor concentration by 80% and testicular responsiveness to LH by 70% 7 days after surgery. Treatment with PRL (75 or 150 µg/day) or with GH (75 or 150 µg/day) initiated within 6 h after surgery and continued twice daily for 6 days partially prevented the loss of LH receptors. The effect of PRL (150 µg/day) plus GH (150 µg/day) on LH receptor concentration was additive. The combination of LH (5 µg/day), PRL, and GH prevented any loss of LH receptors after hypophysectomy. A positive effect of LH on its receptor occurred in the presence of PRL. Treatment of hypophysectomized rats with 5 /µg LH plus 150 /µg PRL enhanced the effect observed with PRL alone (1.31 pmol/testis vs. 1.68 pmol/testis, P < 0.05). We previously reported that administration of 5, 25, or 50 µg LH/day to hypophysectomized rats caused a further decrease in LH receptor concentration (1). In the present study, administration of PRL (150 µg sol;day) together with 25 or 50 µg LH/day prevented LH from exerting a negative effect on LH receptor concentration. Similar treatment with GH plus LH neither allowed a positive effect of LH nor prevented higher doses of LH from exerting a negative effect on LH receptor concentration. Despite the ability of PRL to increase LH receptor concentration, PRL treatments did not enhance testicular responsiveness to LH. Only when LH was administered together with either PRL and/or GH was testicular responsiveness to LH maintained at intact control values. These data indicate that 1) maintenance of testicular LH receptors is at least partially dependent on PRL and GH; 2) PRL prevents LH from exerting a negative effect and allows LH to have a positive effect on its receptor; 3) PRL and GH seem to act at different sites and by different mechanisms; and 4) hormonal regulation of LH receptor concentration is distinct from hormonal regulation of testicular responsiveness to LH.

Footnotes

^* This work was presented in part at the 59th Annual Endocrine Society Meeting, Chicago, IL, July 8-10, 1977. This investigation was supported by NIH Grants HD-08538 and HD-07690.

Fellow of the Department of Pediatrics and Communicable Diseases.

Received November 11, 1977.

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