Prostaglandin F-2 alpha receptors in corpora lutea of pregnant rats and relationship with induction of 20 alpha-hydroxysteroid dehydrogenase.
Luteal receptors for PGF-2 alpha in the pregnant rat were characterized. No changes in the Kd were found during pregnancy, whereas capacity increased to a maximum on Day 19, decreasing thereafter. The decrease in binding sites seen from Days 20 to 22 may be due to down regulation of the receptor by its ligand, since it was prevented by inhibition of PG synthesis by indomethacin treatment. Likewise, in-vivo treatment with PGF-2 alpha reduced the apparent number of PG binding sites. PG receptor concentration seems to be modulated by oestrogens since an increment was found on Day 19, associated with the known increase in plasma oestradiol concentrations, and since receptor concentration on Day 16 was significantly increased by oestradiol benzoate. The uterus also had a negative influence on the appearance of the PG receptor, since hysterectomy on Day 16 increased the number of binding sites on Day 18. However, receptor concentration and 20 alpha-hydroxysteroid dehydrogenase induction by hysterectomy was not affected by indomethacin, indicating that these events are probably not related to prostaglandin withdrawal. However, treatment with hCG, which diminishes enzyme induction by hysterectomy, did not produce changes in receptor concentration. The present results suggest that PGF-2 alpha, acting through a specific receptor site, is the physiological luteolytic signal. The consequence of its receptor binding seems to be the blockade of a gonadotrophic stimulus, which in turn determines (1) the decrease in progesterone synthesis and (2) the induction of 20 alpha-hydroxysteroid dehydrogenase.
Bussmann
L E
LE
Laboratorio de Reproduccion y Lactancia (LARLAC), Mendoza, Argentina.
D015089:20-Hydroxysteroid Dehydrogenases / Q000378:metabolism*; D043607:20-alpha-Hydroxysteroid Dehydrogenase; D000818:Animals; D003338:Corpus Luteum / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism*; D015237:Dinoprost / Q000378:metabolism*; D004958:Estradiol / Q000494:pharmacology; D005260:Female; D007044:Hysterectomy; D007213:Indomethacin / Q000494:pharmacology; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000378:metabolism*; D011374:Progesterone / Q000494:pharmacology; D051381:Rats; D011982:Receptors, Prostaglandin / Q000187:drug effects / Q000378:metabolism*
D011982:Receptors, Prostaglandin; C034671:prostaglandin F2alpha receptor; D011374:Progesterone; D004958:Estradiol; D015237:Dinoprost; D015089:20-Hydroxysteroid Dehydrogenases; D043607:20-alpha-Hydroxysteroid Dehydrogenase; D007213:Indomethacin