The preovulatory gonadotropin surge is regulated by the integrative effects of estradiol and progesterone. Although estradiol is the primary trigger for the preovulatory gonadotropin surge, progesterone exerts important regulating action on the magnitude of the surge. It also plays an important role in limiting the gonadotropin surge to a short duration. The effect of progesterone on gonadotropin secretion may be stimulatory or inhibitory depending upon the time of administration and the dose employed. Adequate estrogen priming is necessary for the stimulatory action of progesterone. The actions of progesterone in initiating a gonadotropin surge include release of neuropeptide Y and gonadotropin releasing hormone (GnRH) from the hypothalamus, suppression of hypothalamic GnRH degradation, and depletion of biologically significant occupied estrogen nuclear receptors of the anterior pituitary. The preovulatory progesterone appears to be of adrenal origin. In the estrogen-primed ovariectomized rat, adrenocorticotropin can induce a gonadotropin surge that is mediated through adrenal progesterone secretion. Naturally occurring corticosteroids, such as deoxycorticosterone, and synthetic corticosteroids, such as triamcinolone acetonide, that interact with the progesterone receptor also can induce gonadotropin surges and ovulation. A variety of progesterone metabolites have biological activity and can bring about luteinizing hormone and/or follicle-stimulating hormone release. They exert their action through either progesterone receptor-mediated mechanisms or membrane effects such as interaction with the γ-aminobutyrate-ergic system. Most of the work in this review was done in the rat; however, steroid effects on gonadotropin secretion in humans and in nonhuman primates have striking similarities; these have been pointed out at appropriate places in the review.
|Original language||English (US)|
|Number of pages||43|
|Journal||Frontiers in Neuroendocrinology|
|Publication status||Published - Jan 1 1991|
ASJC Scopus subject areas
- Endocrine and Autonomic Systems