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Journal of Clinical Endocrinology & Metabolism, Vol 42, 718-728, Copyright © 1976 by Endocrine Society
ARTICLES |
CF Wang, BL Lasley, A Lein and SS Yen
Submaximal doses of LRF, administered over a period of several hours, either by repeated pulses (10 mug at 2 h intervals X 5) or by constant infusion (0.2 mug/min X 4 h), have permitted the assessment of changes in the releasable gonadotropin during the menstrual cycle. Quantitations in the acute releasable and ultimately releasable gonadotropins were made which represent, respectively, the sensitivity and reserve of the gonadotrophs. The functional expression of these two components of gonadotropin release exhibited profound changes during the menstrual cycle and were in synchrony with the cyclicity of ovarian steroid levels; during the early follicular phase, both sensitivity and reserve were at a minimum, but with increasing levels of E2, a preferential increase in reserve over sensitivity (P less than 0.005) was found. Although both sensitivity and reserve increased dramatically near the midcycle, the relative change in these two components was reversed from the late follicular phase to the midcycle surge. The presence of this phenomenon may be causally related to the development of a self-priming effect of LRF at this time, as evidenced by an augmentation of gonadotropin release to the 2nd pulse of LRF. Thus, a build-up in pituitary store consequent to the greater increase in reserve than in sensitivity, together with the appearance of the self- priming effect of LRF induced by progressively rising levels of E2, may constitute the essential dynamics required for the development of the midcycle gonadotropin surge. Pituitary sensitivity and reserve continued to be high during the early luteal phase but reduced progressively thereafter. In all studied, FSH responses were less obvious but showed remarkable parallelism to the pattern of LH responses. We have concluded that the functional capacity of the gonadotrophs exhibits a remarkable cyclic change and that the adenohypophysis represents a critical feedback site in the development of pre-ovulatory gonadotropin surge.
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