The pituitary response to synthetic LH-releasing factor (LRF) has been measured following administration of progesterone (P) or estradiol benzoate (EB) in amounts known to retard or advance ovulation in 4- and 5-day cyclic rats. Charles River CD rats, treated with P or EB SC in oil 3 hr to 2 days earlier and anesthetized with pentobarbital (35 mg/kg, ip) at 1345 hr, were given LRF (75 ng/100 g) via external jugularvein cannula at 1500 hr. Serum LH was measured by radioimmunoassay of samples collected at 0, 10, 30,and 60 min. Administration of P (1 mg/100 g) at noon on diestrus-1 (D-l) converted 4-day cycles to artificial 5-day cycles with a 24-hr delay in ovulation. Theresponsiveness of the pituitary to LRF on day 3 of the extended cycle was significantly less than that of untreated rats in proestrus and was equivalent to that of natural 5-day D-3 animals. By contrast, 5-day cycles were shortened to 4 days with 24-hr advance in ovulation by P (1 mg/rat) at noon on D-3 of the artificial cycle, or by EB (15µg/rat) at noon on D-2 of either the natural or artificial cycle. In all animals, conversion of D-3 to a functional proestrus was accompanied by a significant increase in LH release after administration of LRF. Similarly, when 4-day cycles were shortened to 3 days by EB (20 µg/rat) at 1230 hr on D-l, the pituitary responsiveness to LRF (300ng/100 g) the next day was greater than the normal D-2 response. Thus, advance or delay of spontaneous ovulation by EB or P is demonstrated to be accompanied by a corresponding augmentation or inhibition of pituitary responsiveness to LRF. (Endocrinology95: 1664, 1974)
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Martin et al. (1974) studied this question.