Luteinizing hormone-releasing hormone, ovariectomy, and silastic vaginal rings in the Rhesus monkey.

The interaction of estradiol and luteinizing hormone-releasing hormone (LRH) may be a critical physiologic mechanism regulating the occurrence of ovulation in many species. These studies were conducted to assess (1) the effects of intramuscular injections of LRH in the intact female rhesus monkey and (2) the effects of estradiol in a Silastic delivery system in ovariectomized female rhesus monkeys. No changes in blood levels of luteinizing hormone (LH) were detected in response to 200 micrograms of LRH. Ovulation did not occur 48 hours after treatment. Ovariectomy decreased estradiol, increased LH, and had no effect on prolactin concentrations in sera. Insertion of a vaginal ring containing 10% estradiol increased blood estradiol levels 100-fold. Serum prolactin levels were unaffected; however, LH concentrations were altered in a multiphasic fashion. After the ring had been in place for 15 days, vaginal blood similar to menstrual flow was observed following removal.

PIP: The effects of im injections of luteinizing hormone-releasing hormone (LH-RH) in the intact female rhesus monkey and the effects of estradiol in a Silastic delivery system in ovariectomized female rhesus monkeys are reported. In the 1st study, 4 females received injections of 200 mcg of LH-RH on Day 8 of the menstrual cycle. Blood samples were collected 15 minutes prior to injection and .5, 1, and 2 hours after injection. Samples were analyzed for presence of LH. In the 2nd experiment, ovariectomized animals received replacement therapy via a vaginal ring. Blood samples were obtained on the day of ovariectomy and once weekly for 1 month following surgery. At that time a 10% estradiol ring was inserted and blood samples obtained 3 times/week for 2 weeks. The ring was then removed and samples taken for an additional 1-month period. These same monkeys were again inserted after a 3-month rest period and blood samples collected twice daily 2 days prior to and for 4 days following insertion. The rings were removed on the 4th day, and a final sample taken 3 days later. Sera from the vaginal ring studies were analyzed for LH, estradiol, and prolactin. LH changes in response to injection to 200 mcg of LH-RH were insignificant. Ovulation was absent 48 hours after treatment. Ovariectomy decreased the level of estradiol and increased the LH levels. Replacement therapy increased blood estradiol levels 100-fold. Prolactin levels were unaffected by treatment. When the ring was withdrawn LH levels again increased and estradiol levels decreased. Withdrawal of the estradiol ring was followed by menstrual flow.

Interactions of prostaglandin E1 (PGE1) and LRH on anterior pituitary function.

Numerous biochemical pathways influence the synthesis and release of anterior pituitary hormones. Releasing factors extracted from the hypothalamus and prostaglandins (PGs) appear to alter a common biochemical activity, adenyl cyclase, in pituitary cells. Luteinizing hormone releasing hormone (LRH), prostaglandin (PGE1), 7 oxa-13-prostynoic acid and cycloheximide were tested for individual and interacting effects on the in vitro release of FSH, LH and prolactin from hemipituitaries of 15 day old female rats. LRH (10 ng/ml) consistently released both LH and FSH in all in vitro experiments and inhibited prolactin release in 1 of 2 experiments. Lower concentrations (5 and 1 ng/ml) also stimulated LH and FSH release but did not influence prolactin release. Concurrent depletion of stored LH and FSH in the gland was observed. PGE1 in a 6.5 hour incubation increased the storage of LH within the gland in the absence of LRH. In a 1.5 hour incubation in the presence of LRH, storage of LH was also increased. PGE1 had no effect on LH and FSH release; however, in 1 of 2 experiments it stimulted prolactin release in the absence of LRH. Prostynoic acid stimulted LH and FSH release but did not synergize with LRH action in the same tissue. Cycloheximide did not affect LH release during the first 30 minutes of incubation; however, the release during the subsequent 1 hour was significantly inhibited. Similar tissue also exposed to cycloheximide was still responsive to LRH during the latter 1 hour incubation period. Cycloheximide had no effect on prolactin storage and release from the same tissue.