The Actions of Porcine Follicular Fluid and Estradiol on Periovulatory Secretion of Gonadotropic Hormones in Rats*

Abstract

We investigated 1) if the administration of porcine follicular fluid (p FF) on proestrus could block the entire periovulatory gonadotropin secretion in the 4-day cyclic rat, 2) if the maintenance of elevated serum 17β-estradiol (E₂) concentrations during proestrus and estrus has any influence on periovulatory FSH release, either alone or in combination with pFF, and 3) if the administration of pFF to proestrous rats interferes with LHRH-induced gonadotropin release. We collected blood through a jugular cannula at 4-h intervals from 1400 h on proestrus to 1000 h on estrus and measured the plasma for LH and FSH by RIA. Experimental protocols included injecting pFF at low (0.1 ml) or high (0.5 ml) doses, early (at 1000, 1300, and 1530 h on P), or late (at 1800, 2100, and 2400 h on P), or at all six times, or implanting sc an E₂ Silastic capsule at 1300 h on P. We injected the pFF through the cannula, except for the 1000 h injection which was ip. Either dose ofpFF (early) completely blocked the proestrous increase in plasma FSH observed in normal and pig serum-injected controls, but plasma FSH was only partially suppressed during the morning of estrus during the time a secondary elevation in plasma FSH was observed in controls. Plasma FSH did not rise during estrus when the high dose of pFF was administered late or at all times. If the low dose of pFF was not injected at 1000 h despite its injection at the other five times, a small elevation in plasma FSH was observed throughout proestrus and estrus, and a proestrous LH surge occurred. Interestingly, the LH surge was blocked in most rats which received either dose of pFF if the injection at 1000 h on proestrus was included. E₂ had no effect on the periovulatory gonadotropin surges, and it did not prevent the small rise in plasma FSH during estrus in rats given the low dose of pFF early. Additional rats were ovariectomized and administered phenobarbital on the early afternoon of proestrus. In these rats, plasma LH remained low, and plasma FSH rose by 2200 h on P to levels which were similar to those observed during the secondary rise in plasma FSH during estrus in controls. The high dose of pFF administered six times completely blocked, and the low dose of pFF administered six times suppressed, the elevations in plasma FSH in the phenobarbital-treated ovariectomized rats, and E₂ did not suppress plasma FSH further in phenobarbital-treated ovarectomized rats given the low doses of pFF. Constant rate iv infusion of LHRH at 50 ng/h from 1400–1700 h on proestrus did not elevate plasma FSH in intact rats given the high dose of pFF early, but did cause a partial rise in plasma LH during proestrus compared to values observed in phenobarbital-blocked, LHRH-infused controls. The results suggest that 1) decreasing inhibin titers may be involved in the selective release of pituitary FSH during estrus, 2) decreasing E₂ titers play no major role in the selective release of pituitary FSH during estrus, either alone or in association with decreasing inhibin titers, 3) pFF can block the preovulatory LH surge when administered on the morning of proestrus, and 4) the action of pFF to completely suppress proestrous but not necessarily estrous gonadotropin secretion is probably exerted at the anterior pituitary gland to suppress LHRH-induced gonadotropin release.