Abstract

PIP:

A hypothetical scheme for feedback actions on target hypothalamic and pituitary actions by gonadotropins is proposed, and present state of knowledge in this respect is presented. A stimulatory effect of target organ hormones on the hypothalamo-adenohypophysial system (HAS) was shown only to operate in the case of gonadotropin surge. In spontaneous ovulators, at low plasma progesterone levels, estradiol 1st increases pituitary responsiveness and then permits the expression of a daily neural signal that results in the increased release of gonadotropin-releasing hormone (GRH) into portal vessel blood. Increased GRH in portal vessel blood releases luteinizing hormone (LH), and at the same time further increases pituitary responsiveness by its priming effect. The increased plasma LH concentration stimulates the secretion of progesterone, which further increases pituitary responsiveness. This series of events leads to the LH surge. The priming effect of GRH obviates the need for a massive release of GRH and ensures that the peak of the GRH surge coincides with the peak in pituitary responsiveness. To be affected fully by estradiol and progesterone, the gonadotropins must be exposed to GRH; this is why neural blocking agents can inhibit the effect of these steroids. Secretion of LH but not FSH is dependent on continuous exposure of the gonadotropins to GRH. The factors that terminate the GRH surge are not known, though progesterone may play a role. This scheme also operates in the production of the 1st LH surge in rats.