Abstract
In the rat, the hypothalamic peptide GnRH acts not only at the pituitary but can also modulate ovarian function directly [1, Review]. Recently, a role for a phospholipid- and Ca2+-dependent protein kinase (PK-C) has been suggested in the action of GnRH on the pituitary [2]. GnRH is known to reduce gonadotrophin-stimulated progesterone (P) production by rat luteal cells through the inhibition of hormone-responsive adenylate cyclase [3]. The tumor-promoting phorbol-ester, phorbol 12-myristate 13-acetate (PMA), a well-known activator of PK-C, has been shown to reduce steroidogenesis by mouse Leydig cells through inhibition of hormone-stimulated cAMP formation [4]. In order to determine whether the inhibitory action of GnRH on luteal steroidogenesis is effected through activation of PK-C, we compared the effects of a GnRH agonist, Des-10-Gly-(6Trp)-GnRH-ethylamide (GnRH) on steroidogenesis and cAMP formation by rat luteal cells with those of PMA.
Published Version
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