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Biology of Reproduction, Vol 25, 492-501, Copyright © 1981 by Society for the Study of Reproduction

Prostaglandin F2agr Regulation of LH-Stimulated Testosterone Production in Rat Testis

ANNA-RIITTA FUCHS 1, and UDOM CHANTHARAKSRI 1

1 Center for Biomedical Research, The Population Council, Rockefeller University, New York, New York 10021 and The Graduate School for Medical Sciences, Cornell University Medical College, New York, New York 10021


The effect of PGF2agr on testicular testosterone (T) production and its possible influence on LH action was studied in adult male rats in vivo and in vitro. Various doses of PGF2agr were administered by slow infusion of 4 h duration, and plasma T was determined by RIA in samples obtained through an indwelling cardiac catheter. PGF2agr (250 µg/rat) caused a rapid and consistent fall in plasma T to 50% of initial levels while during similar infusions of saline, plasma T increased by 60% on the average. PGE2 (250 µg/rat) had no significant effect on plasma T. Infusion of anti-LH serum for 4 h reduced plasma T by 72%; infusion of 250 µg/rat of PGF2agr in anti-LH-treated rats did not reduce plasma T further. LH administration (3 and 10, but not 1 mU/rat) overcame the PGF2agr induced drop in plasma T in a dose-dependent manner. Indomethacin treatment (1 or 2 mg/kg for 10 days) caused a significant and sustained elevation in plasma T.

The basal T output by the decapsulated testis preparation in vitro was not affected by either PGF2agr, PGE2 (up to 10-3 and 10-4 M, respectively), anti-LH serum, or prostaglandin synthetase inhibitors, while the LH (25 mU/ml)-stimulated testosterone secretion was inhibited in a dose-dependent manner by PGF2agr and its 15-methyl derivative (ED50 = 6.8 x 10-5 M) and was blocked by anti-LH. Prostaglandin synthetase inhibitors, indomethacin (10-6 M), and diclofenac-sodium (10-4 M), potentiated the stimulatory action of LH or hCG in vitro; this was reversed by PGF2agr.

We conclude that PGF2agr inhibits LH-stimulated testosterone production in Leydig cells. Since PGF2agr production in the testis is stimulated by hCG or LH, we suggest that endogenous PGF2agr acts as a local regulator of LH action in the Leydig cells. The action of PGF2agr on testicular steroidogenesis is thus analogous to its action on rat luteal cells and as in the female, PGF2agr may be of physiological significance in testicular function in male rats.

 Submitted on February 2, 1981
Accepted on May 20, 1981




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[Abstract] [Full Text] [PDF]


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Copyright © 1981 by the Society for the Study of Reproduction.