Hypothalamo-hypophyseo-gonadal axis in individuals with chronic renal insufficiency subjected to hemodialysis

The role of pituitary and sexual hormones in 21 patients with chronic renal failure (CRF) and related impotence and loss of libido who were being treated by hemodialysis and in 15 normal male controls has been studied. In both groups the serum levels of FSH, LH and TSH, PRL before and after injection of both LHRH and TRH were measured as well as the basal levels of Testosterone (T) and Estradiol (E2). The results show similar values for testosterone in both groups and statistically significant higher basal values for FSH, LH, TSH and PRL and lower basal values for E2 in CRF patients.     

Feedback effects of ovarian steroids on the hypothalamic-hypophyseal axis in the rabbit

The feedback effects of two ovarian steroids, estradiol-17 beta (E2) and 20 alpha-hydroxypregn-4-en-3-one (20 alpha OH), were examined in both intact (INT) and ovariectomized (OVEX) does. We measured steroid-induced alterations in endogenous gonadotropin-releasing hormone (GnRH) from sequential 10-min samples of hypothalamic perfusates, simultaneous changes in peripheral plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH), and the modification of pituitary responsiveness, i.e., increments in plasma LH (delta LH) and plasma FSH (delta FSH), after 50 ng, 250 ng, and 1 microgram of exogenous GnRH in individual does of 6 treatment groups. The groups were: INT does, OVEX does, OVEX does receiving either one (1 E2) or two (2 E2) E2-filled Silastic capsules, OVEX does receiving a 20 alpha OH-filled capsule (20 alpha OH), and OVEX does receiving both capsules of E2 and 20 alpha OH (1 E2 + 20 alpha OH). Ovariectomy enhanced the pulsatile release of hypothalamic GnRH and pituitary LH and FSH, and increased the LH response (delta LH) to exogenous GnRH (OVEX vs. INT, p less than 0.05). Replacement of E2 at the time of ovariectomy prevented the increased GnRH and gonadotropin secretion as well as the enhanced delta LH that were observed in untreated OVEX does. The release of hypothalamic GnRH in the 20 alpha OH group was lower (p less than 0.05) than that in the OVEX group and not different from that in the INT group. The release of pituitary LH and FSH and the delta LH in the 20 alpha OH group was not different from that in the OVEX group, but these parameters were greater (p less than 0.05) than those in the INT group. The hypothalamic GnRH pulse frequency in the 1 E2 + 20 alpha OH group was lower (p less than 0.05) than that in either the 1 E2 or the 20 alpha OH group, but the delta LH in the 1 E2 + 20 alpha OH group was not different from that in either the 1 E2 or the 20 alpha OH group. The highest dose (1 microgram) of exogenous GnRH stimulated a modest increase in FSH in the OVEX, 20 alpha OH, 1 E2 + 20 alpha OH, and 1 E2 groups; but a steroid effect on delta FSH among these 4 groups was not apparent.(ABSTRACT TRUNCATED AT 250 WORDS)     

Partial deficiency in 21-hydroxylase in certain forms of hirsutism

The ACTH test is important when hirsutism occurs in women with a slight 21-hydroxylase deficiency, and normal basal 17-OH Progesterone (17-OH-P/plasma levels). Extensive hormonal assays: LH, FSH, Prolactin, 17 beta-estradiol (E2), Estrone, 17OH-P, Androstenedione, Testosterone, Cortisol (C), Dehydroepiandrosterone-S (DEA-S) were carried out in 36 hirsute women. 13 of these presented hormone levels as found in polycystic ovary syndrome (PCOS), 6 women presented a slight 21-hydroxylase deficiency (increased plasma 17-OH-P and decreased C after ACTH test with significant, p less than 0.01, increase of 17-OH-P/C and 17 women presented idiopathic hirsutism (IH). The hormonal pattern, in the basal condition, is not different in IH or in slight 21-hydroxylase deficiency. The ACTH test is able to differentiate between IH and adrenal hirsutism.     

Effect of luteal metoclopramide-induced hyperprolactinemia on pituitary and luteal responsiveness to gonadotropin-releasing hormone

The pituitary and corpus luteum responses to acute gonadotropin-releasing hormone (GnRH) administration at the mid-luteal phase (LP) were studied in 24 infertile women. Patients were randomly divided into two groups. In one group (n = 12) metoclopramide (MCP, 10 mg orally 3 times daily) was administered from day 0 or 1 of the LP for 7 days. On day 7 or 8 of LP blood samples were taken every 15 min for 180 min; then 25 micrograms GnRH were acutely administered intravenously and blood samples taken at 185, 195, 210, 225, 240, 255, 270, 285 and 300 min. In the other 12 patients the same experimental design was performed on day 7 or 8 of an untreated LP. Plasma prolactin (PRL), luteinizing hormone (LH), follicle-stimulating hormone (FSH), progesterone and estradiol (E2) were assayed. The responsiveness of the different hormones to GnRH was evaluated as the integrated secretory area for 120 min after injection (sISA = stimulated integrated secretory area) and as the percentage increase (delta A) with respect to the area under basal conditions before GnRH administration (bISA = basal integrated secretory area). MCP-treated women showed higher basal PRL levels (p less than 0.01) and lower basal plasma concentrations and bISA (p less than 0.01) values of LH than controls. After GnRH a more marked response of LH secretion was observed in the treated group (p less than 0.01), so that the absolute values of sISA were superimposable in both groups. Basal and stimulated FSH secretion did not differ significantly in the study groups. Basal plasma and bISA values of progesterone were also decreased in MCP-treated subjects. After GnRH injection the absolute values of progesterone sISA were greater in controls (p less than 0.01), but delta A values were similar in both groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Negative feedback effects of chlormadinone acetate and ethynylestradiol on gonadotropin secretion in patients with prostatic cancer and male rats

Serum LH and FSH levels were determined before and after LH-RH injection (100 micrograms, i.m.) in patients with prostatic cancer who were chronically treated with either chlormadinone acetate (CMA, 100 mg/day) or ethynylestradiol (EE, 1 mg/day). In patients treated with EE, the levels of serum LH and FSH before and after injection of LH-RH were significantly lower than those in controls. On the other hand in patients treated with CMA, the basal levels of serum gonadotropins did not differ from those in controls, and the increase in gonadotropin after LH-RH injection was comparable to that in controls. To examine the effects of these steroids on the hypothalamo-hypophysial axis in the regulation of gonadotropin secretion, CMA or EE was implanted in castrated male rats. CMA, EE or cholesterol (control) was implanted in the hypothalamic median eminence-arcuate nucleus region through a stainless doublecannula. EE implantation resulted in a 75% decrease in serum LH (p < 0.001) and a 38% decrease in serum FSH (p < 0.05) from the control levels on day 5 of implantation. On the other hand, CMA implantation induced a 33% decrease in serum LH (p < 0.05) from the control level on day 3 of implantation, but no significant change in serum FSH levels. The injection of 2 micrograms/kg of LH-RH on day 7 of implantation induced significant lowering of LH and FSH levels. There was no significant difference between serum levels of the hormones 20 min after LH-RH injection for these two groups and those for the control group. These studies suggest that EE has a potent negative feedback effect on both LH and FSH secretion, and that CMA has a mild negative feedback effect on LH secretion.     

Pituitary gonadotropin-releasing hormone receptor content in rats with polycystic ovaries

A single injection of estradiol valerate (EV) induces, after a lag period of 4-6 wk, a chronic anovulatory polycystic ovarian (PCO) condition in adult rats. This condition is associated with a selective compromise of luteinizing hormone (LH) release and/or synthesis reflected in low basal serum LH concentrations, decreased pituitary content of LH, and decreased gonadotropin-releasing hormone (GnRH)-stimulated LH secretion. The present study was undertaken to determine to what extent the aberrant LH release in rats with PCO could be related to alterations in pituitary content of GnRH receptors. Pituitary GnRH-receptor content was assessed by the evaluation of saturation binding of a GnRH analog, [125I]-D-Ala6-des-Gly10-GnRH, to pituitary membrane preparations. The receptor content of pituitaries from rats with PCO was compared to that obtained from intact animals at estrus and diestrus. Receptor levels in ovariectomized normal rats and rats with PCO were also assessed. The pituitary GnRH receptor content in PCO rats was similar to that observed in normal controls at estrus and was significantly lower than that for rats at diestrus. Although a twofold increase in pituitary GnRH receptor content was observed at 28 days following the castration of control rats, GnRH receptor content in the pituitaries of PCO rats, at 28 days following ovariectomy, remained unchanged. Although, castration-induced elevations in mean serum LH and follicle-stimulating hormone (FSH) concentrations were observed in both the PCO and control animals, the rise in both gonadotropins was significantly attenuated in the PCO-castrates when compared to the ovariectomized controls. Since GnRH is a major factor in the regulation of pituitary GnRH receptor content, these findings suggest that hypothalamic GnRH release is impaired in rats with PCO and that this impairment is independent of any influences from the polycystic ovaries.     

Changes in gonadotrope responsivity to gonadotropin releasing hormone during development of the rhesus monkey

To assess the changing responsiveness of pituitary gonadotropes to gonadotropin releasing hormone (GnRH) during development, 5 male and 5 female rhesus monkeys were studied. Three monkeys of each sex were tested periodically with a subcutaneous injection of 500 micrograms of GnRH dissolved in 50% polyvinylpyrrolidone (PVP) beginning at 2 to 4 weeks of age and continuing into young adulthood. The remaining 4 monkeys received injections of the vehicle (PVP) alone and served as controls. Serum concentrations of bioactive luteinizing hormone (LH) were determined by an interstitial cell testosterone bioassay, and follicle-stimulating hormone (FSH) levels were measured by radioimmunoassay. Baseline FSH levels in the 5 female neonatal monkeys were higher than those of the 5 male neonatal monkeys during the first 2 months of life. In both sexes, FSH concentrations decreased with age, and FSH was barely detectable by 6 months. Baseline LH values in the 5 female monkeys declined during the first 6 months of the study and were undetectable (less than 0.5 micrograms/ml) at 6 months of age. Baseline LH levels in 4 of the 5 neonatal males also declined to undetectable concentrations by 6 months of age. During the first 3 months of life, there was a striking increase in the serum concentrations of both LH and FSH following GnRH. Although the LH responses to GnRH (delta LH) were similar in males and females of comparable ages, the FSH responses (delta FSH) were considerably greater in the female monkeys. In the males, the delta LH exceeded the delta FSH, whereas in the females, the delta FSH were greater than the delta FSH. In both sexes, the delta LH and delta FSH generally were greatest in the youngest monkeys and decreased gradually with increasing age. By 6 months, the gonadotropin responses to GnRH either were undetectable (males) or very small (females). After 6 months there was no longer an increase in serum gonadotropins after GnRH in either sex until 1.5-4 years (females) or 3 years (males) of age. The delta LH in response to GnRH in the male monkeys 3-5 years of age were comparable to the responses during the first month after birth. Serum concentrations of FSH in the adult males, however, did not increase after GnRH. In the female monkeys, serum levels of LH and FSH increased after GnRH at 1.5 years (1 monkey) and 4 years (2 monkeys) of age. The delta LH were similar to those of the 1- to 2-month-old female monkeys. The delta FSH, however, were variable and were approximately 20% of the neonatal response. In these young adult female monkeys the delta LH exceeded the delta FSH.(ABSTRACT TRUNCATED AT 400 WORDS)     

Effect of dexamethasone on plasma concentrations of LH, FSH and testosterone in women with hirsutism.

Thirty sexually mature women with hirsutism were treated with 3 x 1.5 mg dexamethasone per day over a period of three days. Before and after treatment, plasma concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH), and testosterone were determined. While an effect of dexamethasone on LH plasma levels could not be established statistically, FSH and testosterone plasma concentrations decreased significantly in comparison to their initial values (p less than 0.01). Special attention is directed to the different effects of dexamethasone on LH and FSH plasma concentrations.     

The role of estrogen in the feedback regulation of follicle-stimulating hormone secretion in the female rat

Letrozole (CGS 20267) is a non-steroidal aromatase inhibitor which, at its maximally effective dose of 1 mg/kg p.o., elicits endocrine effects equivalent to those seen after ovariectomy. Adult, female cyclic rats were administered letrozole (1 mg/kg p.o.) once daily for 14 days. A control group of animals was ovariectomized on day 1 of treatment and a third group of animals served as untreated controls. During the experiment, vaginal smears were taken daily and at the end of 14 days all animals were sacrificed, trunk blood was taken for serum estradiol, LH and FSH measurements and the uterus and ovaries were removed and weighed. The ovaries were then fixed and prepared for histological examination. Serum hormone measurements showed that after treatment with letrozole, serum estradiol levels were reduced by 76% of untreated controls and serum LH was elevated to 378% of control values. These compared favorably with those seen after ovariectomy, serum estradiol was reduced by 78% and serum LH was elevated to 485% of untreated controls. However, FSH was unchanged after letrozole treatment (125% of control), whereas after ovariectomy FSH rose to 398% of control. Uterine weight was suppressed in the letrozole-treated animals as well as the ovariectomized animals by 60 and 70%, respectively. The histology of the ovaries of animals treated with letrozole were consistent with the serum hormone findings. Except for the effects on serum FSH, these results confirm previous findings that treatment with letrozole elicits endocrine effects similar to those seen after ovariectomy. Furthermore, these results demonstrate that FSH secretion is not under the control of estradiol whereas LH secretion is under feedback control of ovarian estrogen.     

Neonatal release of gonadotropins is essential for development of ovarian follicle-stimulating hormone receptors

In the rat, ovarian follicle-stimulating hormone (FSH) receptors increase markedly during the first two postnatal weeks, when serum gonadotropin levels are most elevated. This study was conducted to evaluate the hypothesis that these high gonadotropin levels, and in particular FSH, are involved in the acquisition of FSH receptors by the developing ovary. Gonadotropin release was suppressed by administration of several non-aromatizable androgens, among which dihydrotestosterone propionate (DHTP) was the most effective. In one series of experiments the steroids were administered from Days 5 to 11, and serum FSH and luteinizing hormone (LH) were measured on Day 12. Surprisingly, FSH receptor content was greater in rats with suppressed serum gonadotropins than in controls. The greatest increase in available receptors was observed in DHTP-treated rats in which serum FSH was reduced to 20% of control values and LH suppressed to undetectable values. DHTP failed to directly increase available FSH receptors in hypophysectomized immature rats. Magnesium chloride (MgCl2) treatment of ovarian membranes removed bound 125I-hFSH by 87% without affecting receptor viability. Exposure of control 12-day-old ovaries to MgCl2 increased available FSH receptors to a level similar to that of ovaries from DHTP-treated rats not exposed to MgCl2, suggesting that more receptors were available in DHTP-treated rats because serum FSH was suppressed. Earlier initation of DHTP treatment (postnatal Day 1) suppressed serum FSH and LH to undetectable values by Day 5 and decreased FSH receptor content below control values by Day 12. MgCl2 treatment only slightly increased available receptors in these DHTP-treated animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Gonadotropin secretion during prolonged hyperprolactinemia: basal secretion and the stimulatory feedback effect of estrogen

Inoculation of cyclic female rats with the prolactin (Prl)/growth hormone-secreting pituitary tumor, MtT.W15, resulted in a cessation of estrous cyclicity within 5--10 days. Associated with this acyclicity was a persistently low serum concentration of estradiol and marked increases in both circulating Prl and progesterone. At Day 26 of acyclicity, basal serum luteinizing hormone (LH) values measured in samples taken every 20 min from 0900--1100 h were significantly reduced when compared to cyclic, nontumor animals on diestrus Day 2. There was no difference in basal follicle-stimulating hormone (FSH) concentrations. In a separate group of acyclic, tumor-bearing females 42--56 days after transplantation, a single s.c. injection of 20 micrograms estradiol benzoate (EB) at 1030 h elicited significant increases in both serum LH and FSH values between 1700 and 1830 h on the next day. The magnitude of the LH surge was reduced and that of FSH was increased in tumor-bearing animals when compared to cyclic, nontumor females given a similar EB injection on diestrus Day 1. These results demonstrate that chronic hyperprolactinemia is associated with inhibition of basal LH secretion and ovarian estrogen production and an increase in circulating progesterone concentrations. Nevertheless, the stimulatory feedback effects of estrogen on LH and FSH release are still present and functioning in acyclic female rats under chronically hyperprolactinemic conditions. These data suggest that the cessation of regular ovulatory cycles associated with hyperprolactinemia may be due to a deficiency of LH and/or estrogen secretion, but not to a lack of central nervous system response to the stimulatory feedback action of estrogen.     

Plasma gonadotropin patterns characterizing the development of polycystic ovaries in the estradiol valerate treated rat

Polycystic ovaries (PCO) develop in female rats within 4 weeks of an injection of estradiol valerate (EV). The final morphological transition from a noncystic to a cystic state occurs in the presence of estrous (control) mean serum gonadotropin concentrations, suggesting that gonadotropin patterns rather than mean concentrations are causal to PCO. We have examined plasma luteinizing hormone (LH) and follicle-stimulating hormone (FSH) patterns in female rats at estrus and on days 5, 11, 16, and 21 following EV treatment. Estrous animals displayed large amplitude LH pulses of short duration, interspersed among frequent, low amplitude pulses of similar duration, and infrequent, broad-based LH episodes. Following EV treatment, there was a progressive decline in the frequency and magnitude of the large amplitude LH pulses, such that by day 16, they ceased altogether. Conversely, the frequency of the low amplitude pulses increased such that the total pulse frequency remained constant. The onset of this pattern coincides with the wave of atresia that precedes the emergence of cystic follicles. The pulsatile plasma pattern of FSH seen at estrus remained unaltered at all time intervals examined after EV treatment. We conclude that there is a specific LH pattern responsible for the generation and maintenance of the PCO condition.     

Evaluation of sturgeon follicle-stimulating hormone, luteinizing hormone, estradiol, progesterone and testosterone in Acipenser persicus serum to identify fertile broodstock

Various methods have been proposed for the selection of suitable sturgeon broodstock for artificial reproduction. In this study, serum levels of reproductive hormones, namely sturgeon homologues of follicle stimulating hormone (FSH), luteinizing hormone (LH), testosterone (T), estradiol (E2) and progestrone (P), were measured by radioimmunoassay (RIA) in 36 mature broodstock before and after injection of pituitary extract, and the results correlated with sex, age and oocyte polarization index (p). Mature males were significantly younger than females, and showed significant differences in serum P and T levels following pituitary extract injection, although not before that. A significant difference was found between LH, E2 and T before and after injection in the female group. There was also a significant difference between serum levels of T and P in the fertile and infertile groups. Stepwise discriminant function analysis was used to discriminate between fertile and infertile groups. The function had 93,8% overall correct classification, i.e. amongst 100 female broodstock fish, almost 94% of them would be correctly allocated to the relevant group. So the proposed model provides a reliable method for selecting suitable broodstock fish.     

Evidence for a major role of inhibin in the feedback control of FSH in the male rat

Adult rats (16-18/group) received a single intratesticular injection of 25, 100 or 400 microliters glycerol solution (7:3 in distilled water, v/v). Half of the rats in each group were given implants of testosterone, a testosterone-filled Silastic capsule (1.5 cm length) to provide serum values of testosterone within the normal range. After 1 week all animals were killed by decapitation. Serum concentrations of gonadotrophins, testosterone and immunoactive inhibin as well as testicular concentrations of testosterone and bioactive inhibin were determined. Testicular histology was studied in Paraplast-embedded tissue stained with PAS and haematoxylin-eosin. Glycerol treatment caused a dose-dependent ablation of spermatogenesis in a distinct area around the site of injection. Serum concentrations of FSH increased proportionally with increasing spermatogenic damage while serum LH and testosterone remained unaltered except with the highest glycerol dose. The rise in serum FSH was significantly correlated with serum (r = -0.70, P less than 0.001) and testicular (r = -0.66, P less than 0.001) concentrations of inhibin. A less pronounced correlation was found between LH and serum inhibin (r = 0.48). No correlation was found between the concentrations of LH and testicular inhibin or between serum concentrations of FSH and serum testosterone in the 25 and 100 microliters groups. Maintenance of low to normal serum testosterone concentrations by means of Silastic implants blocked the elevation of FSH in glycerol-treated animals but failed to affect significantly serum FSH in untreated rats. In all testosterone treated rats testicular inhibin concentrations were markedly reduced in the presence of lowered concentrations (7-14%) of testicular testosterone and unaltered serum FSH concentrations.     

Activity of the hypothalamo-pituitary ovarian axis in hypothyroid rats with or without triiodothyronine replacement

The hypothalamic pituitary ovarian axis in adult female rats with 131-I induced hypothyroidism was studied before and after triiodothyronine (T3) replacement. Forty days after 131-I, hypothyroid (H) rats showed irregular cycles with predominantly diestrous vaginal smears, atrophied and underweight ovaries, and decreased serum T3, T4, LH and estradiol (E2). T3 replacement restored normal cycles and ovary weight and increased serum E2 levels above control values, while LH levels remained below the limit of detection of the RIA. The GnRH stimulation test performed on the day that the rats exhibited diestrous vaginal smears elicited a greater increase in FSH than in LH in H rats and a greater increase in LH than in FSH in both H-T3 treated and control rats. The data suggest that the lack of thyroid hormones in adult female rats seems to produce a reversion of sexual hormones to a prepubertal pattern, while T3 treatment restored normal estrous cycles and ovarian function.     

Systematic studies invalidate the neonatally androgenized rat as a model for polycystic ovary disease

As an adult, the neonatally androgenized (AZ) rat is anovulatory and exhibits follicular cysts. Thus, the AZ rat has been used as a model for polycystic ovary disease (PCO). However, its correlation with the human disease is not clear; so we have studied the AZ rat to determine its suitability as a PCO model. In Experiment I, reproductive hormones were measured at specific intervals between postnatal Days 15 and 90 in saline-treated and AZ rats. In Experiment II, AZ rats were treated with exogenous follicle-stimulating hormone (FSH) or subjected to unilateral ovariectomy (ULO) as analogies to therapies that have been used to treat human PCO. The results demonstrate that the luteinizing hormone (LH), FSH, testosterone (T), and estradiol (E2) concentrations of the AZ rat were not different from control values. Additionally, FSH therapy did not increase the E2 concentrations or the ovarian weight of the AZ rat. Furthermore, control and AZ rats exhibited similar post-ULO rises in FSH, but compensatory ovarian hypertrophy was not evident in the AZ rat. We conclude that 1) the hormonal and morphological patterns observed in the AZ rat do not correlate with those of PCO and 2) the androgenized rat does not provide an adequate model to study PCO.     

Body composition characteristics, sex hormone levels and circadian gonadotropin fluctuations in infertile young women

The present study dealt with the interaction between body composition estimated by means of dual energy x-ray absorptiometry, sex-specific fat distribution and sex hormone levels (LH, FSH, estradiol, prolactin, DHEA-S, androstendione, testosterone and SHBG) as well as LH and FSH fluctuations in infertile young women ageing between 18 and 30 years (x = 23.4 yr). Twenty patients suffered from polycystic ovaries (PCO), 15 women suffering from a mild anorexia nervosa were amenorrhoeic for more than one year. Marked associations between estradiol, testosterone, SHBG as well as the FSH output and body fat, bone mass and fat distribution were documented. PCO patients exhibited a high weight status and a typical android fat distribution which signals infertility comparable to postmenopausal women. In contrast, although anorexia patients had pathological decreased estrogen levels and were infertile at the time of investigation, their fat distribution was be classified as 'ypergynoid' and signals potential reproductive capability after a sufficient weight gain.     

Exploration of hirsutism: elements for a strategy

50 women complaining of hirsutism were investigated in order to establish an optimal strategy for hirsutism exploration. Basal hormonal evaluations were of great value, especially serum testosterone and, to a lesser degree, DHA-S and LH. LH response to LHRH stimulation appeared of little diagnostic value. ACTH stimulation tests may be useful in detecting enzyme deficiencies in patients with normal basal values. The origin of hyperandrogenism can hardly be detected by the inhibition tests. However, these tests allow to determine whether the androgen secretion is still under ACTH and/or LH control.     

An acute increase in serum prolactin does not modify gonadotropin release in female rats

Attempts were made to find out whether hyperprolactinemia has an effect on the hypothalamo-pituitary response to estrogen feedback and LHRH stimulation. Adult female rats of Wistar strain were ovariectomized and received subcutaneous injection of 20 micrograms estradiol benzoate (EB) 3-4 weeks later (day-0). A second injection of 20 micrograms EB, when administered at noon on day-3, induced a highly significant increase in serum LH (p less than 0.001 vs. basal values), but not FSH, estimated at 1800 h on the same day. This EB-promoted LH release was not altered by pretreatment with rat PRL (5 micrograms/day), which was administered subcutaneously daily in the morning (1100 h) between day-1 and day-3. No statistical difference in the serum LH concentration was found when compared with the values for the control animals pretreated with 0.9% saline alone. Serum gonadotropins 15 min after LHRH administration (100 ng/100 g BW) in 32-day-old female rats were not statistically different between the animals pretreated with 5 micrograms PRL, which was given subcutaneously daily (at 0800 h) for 3 days, and the controls pretreated with 0.9% saline. These results suggest that an acute increase in serum PRL may not exert a negative effect on the gonadotropin release induced by estrogen feedback and LHRH stimulation.     

Daily rhythms of serum luteinizing hormone in the immature hamster are estradiol-dependent

In the female Syrian hamster (Mesocricetus auratus), daily rhythms of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) begin several weeks before regular vaginal estrous cycles are initiated. These rhythms, which appear rather abruptly at about 16 days of age, are dependent on the presence of the ovaries. The experiments described here were intended to determine the nature of the ovarian information required for the initiation and maintenance of the daily LH surge. This surge characterizes the daily cycle of LH and occurs each afternoon at about 1700 h in the intact animal between 2 and 5 weeks of age. Females were ovariectomized at 14 or 15 days of age and implanted with constant-release Silastic capsules of estradiol (E) or progesterone (P). Blood samples were collected at 21 days of age at 1400 or 1700 b, and the serum was assayed for LH, P, and E. While ovariectomy abolished the afternoon surge of serum LH that was observed in sham-operated controls, implantation of E effectively replaced the ovaries. Implantation of P was without effect on LH levels; when P plus E was implanted, the effect was similar to that of E alone. These results suggest that ovaries of the 2-week-old hamster secrete estrogen necessary for the initiation of cyclical LH release.