Serum Luteinizing Hormone Response Research Articles

LHCGR Gene Analysis in Girls with Non-Classic Central Precocious Puberty.

Luteinizing hormone (LH) is a useful parameter in diagnosing precocious puberty. The pubertal response of serum LH to a GnRH stimulation test is varied, and clinical symptoms of precocious puberty are sometimes disproportionate with serum LH concentrations. Many patients present in a state of precocious puberty that advances rapidly, but the post-GnRH peak LH remains prepubertal. LH receptor mutations are suspected of involvement in the non-classic type of central precocious puberty (CPP). To examine the association between LHCGR polymorphism and non-classic CPP in subjects exhibiting a peak LH<5 IU/L on a GnRH stimulation test. In total, 102 girls with non-classic CPP and 100 normal adult women were enrolled. All subjects underwent LHCGR gene analysis by the Sanger method, and patients and controls were compared. Auxological data and gonadotropin concentrations were analyzed in the 102 patients. Of these patients, 75 completed GnRH agonist treatment, and the treatment outcomes were analyzed. A total of seven variants were identified, including two missense mutations (g.48698754 G/A and g.48688613 G/A) that were found in the patient group (no patients contained both mutations). In silico analysis of these missense mutations suggested the possibility of damaging the LHCGR. However, no significant association was found between the identified LHCGR variants and non-classic CPP. GnRH agonist treatment decreased bone age advancement and increased predicted adult height. LHCGR gene polymorphisms do not appear to be a major causative factor for the relatively low concentration of LH in patients with non-classic CPP. GnRH agonist treatment improved clinical parameters in these patients.

Resumption of menstruation and pituitary response to gonadotropin-releasing hormone in functional hypothalamic amenorrhea subjects undertaking estrogen replacement therapy.

Functional hypothalamic amenorrhea (FHA) refers to a functional menstrual disorder with various causes and presentations. Recovery of menstrual cyclicity is common in long-term follow-up but the affecting factors remain unknown. To explore factors affecting the menstrual resumption and to evaluate the pituitary response to gonadotropin-releasing hormone (GnRH) in FHA. Thirty cases with FHA were recruited. All subjects were put on continuous 1 mg/day estradiol valerate orally and followed up monthly. Recovery was defined as the occurrence of at least three consecutive regular cycles. Responder referred to those who recovered within two years of therapy. Gonadotropin response to the 50 μg GnRH challenge was tested every three months. Nineteen (63.3%) subjects recovered with a mean time to recovery of 26.8 months. Time to recovery was negatively correlated with body mass index (BMI) before and by amenorrhea. Twentyone cases had undertaken therapy for more than two years and 10 of them recovered. BMI before and by amenorrhea were negatively correlated with the recovery. Significant increase of serum luteinizing hormone (LH) and LH response to GnRH were noted after recovery. Menstrual resumption was common in FHA undertaking estrogen replacement therapy (ERT). The likelihood of recovery was affected by their BMI before and by amenorrhea but not by the weight gain during therapy. Low serum LH and attenuated LH response to GnRH were the main features of pituitary deficiency in FHA. The menstrual resumption in FHA was accompanied by the recovery of serum LH and the LH response to GnRH.

Evaluation of the Buserelin Stimulation Test in Diagnosing Gonadotropin Deficiency in Males with Delayed Puberty

To assess the efficacy of the gonadotropin-releasing hormone (GnRH) agonist buserelin in a stimulated gonadotropin test for the investigation of delayed puberty in males. Prepubertal males (n = 31; age range, 10.3 to 17.2 years) were studied; buserelin (100 microg) was administered subcutaneously, with blood sampling at 0 and 4 hours for serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH). At follow-up (mean, 4.2 years), 8/31 (26%) failed to progress into puberty, constituting hypogonadotropic hypogonadism (HH), but 23/31 (74%) had testicular enlargement (> or =8 mL) consistent with a normal hypothalamic-pituitary-gonadal (HPG) axis. Stimulated serum LH response to buserelin was lower in males with HH (mean +/- standard error under the mean for HH, 1.4 +/- 0.5 U/L, compared with a normal HPG axis of 17.4 +/- 2.0 U/L; P < .0001). Stimulated serum FSH response was nondiscriminatory (HH, 7.7 +/- 2.2 U/L; normal HPG axis, 11.5 +/- 1.6 U/L; P = .27). All males with HH had a stimulated serum LH level <5 U/L, whereas only 1/23 with a normal HPG axis had a stimulated serum LH below this level. Using this value as the criterion for diagnosing HH, the buserelin stimulation test yielded a sensitivity of 100%, specificity of 96%, and positive predictive value of 89%. The buserelin stimulation test is a highly specific and sensitive GnRH agonist test for the investigation of males with delayed puberty.

The long-term effect of recombinant methionyl human leptin therapy on hyperandrogenism and menstrual function in female and pituitary function in male and female hypoleptinemic lipodystrophic patients

Lipodystrophy patients are hypoleptinemic and insulin resistant. Women have enlarged polycystic ovaries, hyperandrogenism, and amenorrhea. We have determined the role of correction of hypoleptinemia on these metabolic and neuroendocrine parameters. Ten females and 4 males with generalized lipodystrophy were treated with recombinant methionyl human leptin (r-metHuLeptin) in physiologic doses in an open-labeled study for a period of 12 and 8 months, respectively. In the female group, serum free testosterone decreased from 39.6 ± 11 to 18.9 ± 4.5 ng/dL ( P < 0.01) and serum sex hormone binding globulin increased from 14 ± 2.5 to 25 ± 4.8 nmol/L ( P < 0.02). Luteinizing hormone (LH) responses to LH releasing hormone were more robust after therapy and significantly changed in the youngest group of 3 female patients ( P < 0.01). Ovarian ultrasound showed a polycystic ovarian disease pattern in all patients and did not change after therapy. Eight of the 10 patients had amenorrhea prior to therapy and all 8 developed normal menses after therapy. In the male group, serum testosterone tended to increase from 433 ± 110 to 725 ± 184 ng/dL ( P = 0.1) and sex hormone binding globulin also increased from 18.25 ± 2.6 to 27 ± 1.7 nmol/L ( P < 0.04) following r-metHuLeptin therapy. Serum LH response to LH releasing hormone did not show significant changes. Five additional hypoleptinemic male subjects with minimal metabolic abnormalities underwent normal pubertal development without receiving r-metHuLeptin therapy. In both genders, insulin-like growth factor increased significantly and there were no differences in growth hormone, thyroid, or adrenal hormone levels following r-metHuLeptin therapy. Glycemic parameters significantly improved after r-metHuLeptin therapy in both groups. Hypoglycemic medications were discontinued in 7 of 12 patients and dramatically reduced in 5 patients. r-metHuLeptin therapy plays an important role in insulin sensitivity. In females, it plays an additional role in normalizing menstrual function. This is likely to occur both from increasing insulin sensitivity and from restoring LH pulsatility. The persistent hypoleptinemic state in these subjects did not inhibit pubertal development.

Stimulation of luteinizing hormone secretion by N-methyl-D,L-aspartic acid in the adult male guinea-pig: incomplete blockade by gonadotropin-releasing hormone receptor antagonism.

Stimulation of luteinizing hormone (LH) secretion by N-methyl-D,L-aspartic acid (NMA), reported for several mammalian species, is generally accepted to be mediated through stimulation of hypothalamic gonadotropin-releasing hormone (GnRH) release. In view of a previously reported unexpected inhibitory action of NMA on GnRH release from hypothalamic explant of intact male guinea-pigs, the aim of the present study was to assess the in vivo effects of NMA in the adult male guinea-pig. In the gonadally intact male, NMA (5 mg/animal) elicited a robust LH secretion, which was blocked by the N-methyl-D-asparte-receptor antagonist DL-2-amino-5-phosphonovaleric acid (AP-5,12 mg/animal). In the castrated male, NMA elicited only a marginal and inconsistent LH secretion. Cetrorelix (CET), a GnRH receptor antagonist, administered intracardiacally 1 min or 45 min preceding bolus injection of NMA significantly reduced the LH response to NMA in the intact male. Surprisingly, following GnRH receptor blockade with CET, there still was a substantial residual serum LH response to NMA, while CET completely abolished the serum LH response to high dose (1 microg or 10 microg) guinea-pig GnRH (gpGnRH). These results indicate that NMA stimulates LH secretion in the gonadally intact male guinea-pig in vivo and that this effect is mediated in part through gpGnRH-independent mechanisms.

Marked species specificity of guinea pig luteinizing hormone: validation of a bioassay.

The Guinea pig is a potentially interesting alternative small animal model for the study of the neuroendocrine regulation of reproduction. However, appropriate gonadotropin assays are not widely available for this species. The aim of the present study was to validate a bioassay procedure for guinea pig luteinizing hormone (LH). The well-established interstitial cell-testosterone in vitro bioassays with the use of dispersed mouse or rat Leydig cells, successfully applied for measurement of LH from a variety of mammalian species, were found to be unsuitable for assay of guinea pig LH because of a marked species specificity of guinea pig LH. An alternative bioassay procedure was established with the use of dispersed guinea pig Leydig cells. This assay has been shown to allow for the assessment of serum LH response to exogenous gonadotropin-releasing hormone and of the expected spontaneous pulsatile pattern of basal LH secretion, with an apparent mean serum LH pulse interval of 31.4 minutes and 51.9 minutes, in long-term castrated and sham operated male guinea pigs, respectively. This bioassay can be a useful tool for more intensive exploration of guinea pig reproductive physiology.

Persistent Suppression of the Pituitary-Gonadal System in Female Rats by Three-Month Depot Injectable Microspheres of Leuprorelin Acetate

The serum drug levels and pharmacological effects of leuprorelin acetate (leuprolide acetate) in female rats after subcutaneous (sc) injection of 3-month release injectable and biodegradable micro-spheres were investigated. After sc injection, the microspheres provided sustained serum drug levels for >3months, probably because of continuous release of the drug. As was found for the 1-month depot preparation, a transient initial high peak in serum leuprorelin levels resulting from an initial burst of drug release could not be avoided. Sustained suppression of serum luteinizing hormone (LH), follicle-stimulating hormone (FSH), and estradiol for >16weeks was attained by a single injection of the microspheres. An injection of the microspheres suppressed the growth of the ovaries and uterus in a dose-dependent manner; a drug dose of 0.036mg (corresponding to ∼1 µg/kg/day) was insufficient for suppression of uterine growth, and a drug dose of 3.6mg (corresponding to ∼100 µg/kg/day) provided the strongest growth suppression in both organs. Serum LH, FSH, and estradiol responses in a challenge test indicated that definite pharmacological effects were sustained for at least 16weeks, as was demonstrated previously in male rats and dogs. Thus, this depot formulation may provide sustained therapeutic effects for 3 or 4months in humans.

The pituitary gonadotropin-releasing hormone (GnRH) receptor of the female rabbit: characterization and developmental aspects.

The aim of the present study was to characterize the pituitary gonadotropin-releasing hormone (GnRH) binding site in the rabbit and investigate its possible role in sexual maturation of the female rabbit. A radioligand binding assay was established, and the presence of specific 125I-labelled D-Ala6-des-Gly10-GnRH ethylamide (125I-DAl6EA) binding sites in the anterior pituitary gland of the rabbit was demonstrated. 125I-DAla6EA binding was saturable, specific, displaceable, reversible, correlated with increasing tissue concentrations, and susceptible to physiological manipulation. 125I-DAla6EA binding indicated the presence of two binding sites in the female adult rabbit pituitary: a high affinity, low capacity site (KD = 0.3-0.4 nM; Bmax = 100-200 fmol/mg protein) and a lower affinity, high capacity site (KD = 30 nM; Bmax = 5-8000 fmol/mg protein). Ontogeny of 125I-DAl6EA binding in the female rabbit (40-120 days of age) did not show a correlation between binding site number and serum luteinizing hormone (LH). In addition, the net serum LH response in female rabbits to a subcutaneous injection of DAla6EA (10 ng, 100 ng, and 1 microgram per kilogram body weight) was not significantly different between animals 40, 75, and 120 days of age. This suggests that a decrease in pituitary responsiveness to GnRH is not associated with sexual maturation in the female rabbit. Results indicate that factors other than and (or) in addition to GnRH binding site number, such as postreceptor events, play a role in gonadotropin secretion in the female rabbit.

Body weight, hyperinsulinemia, and gonadotropin levels in the polycystic ovarian syndrome: evidence of two distinct populations

To investigate the impact of body weight (BW) and insulin levels on gonadotropin and androgen levels in women with the polycystic ovarian syndrome (PCOS). Comparative study of endocrinologic parameters in PCOS women. University Hospital Reproductive Endocrinology Unit. Thirty obese and 19 nonobese women with PCOS. Seven obese and 7 nonobese normal women. Serum concentrations of insulin, testosterone, androstenedione, luteinizing hormone (LH), follicle-stimulating hormone. Serum LH response to gonadotropin-releasing hormone (GnRH) administration and assessment of insulin resistance by the continuous infusion of glucose with model assessment (CIGMA) test. Fasting insulin levels correlated with body mass index (BMI). Basal LH levels correlated inversely with BMI. Nonobese women with PCOS had a higher LH response to GnRH than obese women with PCOS. Only obese women with PCOS showed insulin resistance and fasting hyperinsulinemia. The data suggest that women with PCOS may be divided into two subgroups: those with obesity, insulin resistance, hyperinsulinemia, and normal/minimally elevated LH levels and those with normal BW, elevated LH levels, and normoinsulinemia.

Effects of suckling and of a long interval after ovariectomy on hypothalamo-hypophyseal responsiveness to naloxone, morphine and GnRH in beef cows

The response of serum luteinizing hormone (LH) to morphine, naloxone and gonadotropin-releasing hormone (GnRH) in ovariectomized, suckled (n=4) and nonsuckled (n=3) cows was investigated. Six months after ovariectomy and calf removal, the cows were challenged with 1mg, i.v. naloxone/kg body weight and 1 mg i.v. morphine/kg body weight in a crossover design; blood was collected at 15-minute intervals for 7 hours over a 3-day period. To evaluate LH secretion and pituitary responsiveness, 5 μg of GnRH were administered at Hour 6 on Day 1. On Days 2 and 3, naloxone or morphine was administered at Hour 3, followed by GnRH (5 μg/animal) at Hour 6. Mean preinjection LH concentrations (3.6 ± 0.2 and 4.7 ± 0.2 ng/ml), LH pulse frequency (0.6 ± 0.1 and 0.8 ± 0.1 pulses/hour) and LH pulse amplitude (2.9 ± 0.5 and 2.9 ± 0.6 ng/ml) were similar for suckled and nonsuckled cows, respectively. Morphine decreased (P < 0.01) mean serum LH concentrations (pretreatment 4.2 ± 0.2 vs post-treatment 2.2 ± 0.2 ng/ml) in both suckled and nonsuckled cows; however, mean serum LH concentrations remained unchanged after naloxone. Nonsuckled cows had a greater (P < 0.001) LH response to GnRH than did suckled cows (area of response curve: 1004 ± 92 vs 434 ± 75 arbitrary units). We suggest that opioid receptors are functionally linked to the GnRH secretory system in suckled and nonsuckled cows that had been ovariectomized for a long period of time. However, gonadotropin secretion appears not to be regulated by opioid mechanisms, and suckling inhibits pituitary responsiveness to GnRH in this model.

Hypothalamic luteinizing hormone-releasing hormone content and serum luteinizing hormone levels in male rats during wallerian degeneration of sympathetic nerve terminals after superior cervical ganglionectomy

The main hypothesis of this study was that sympathetic neurons located at the superior cervical ganglia (SCG) control luteinizing hormone (LH) releasing mechanisms by acting at a hypothalamic site. To test this, medial basal hypothalamus (MBH) luteinizing hormone-releasing hormone (LHRH) content and serum LH levels were measured in male rats subjected to superior cervical ganglionectomy (SCGx) or sham-operation 14 or 38 h earlier, at the time of degeneration of nerve endings post-SCGx. Significantly augmented MBH LHRH levels and decreased circulating LH were found in SCGx rats. In animals subjected to SCGx 14 h earlier and receiving a single injection of the alpha 1-adrenergic blocker prazosin, the beta-adrenergic blocker propranolol or a mixture of both drugs 45 min before sacrifice, only the injection of prazosin prevented the decrease of plasma LH levels. Neither treatment prevented the increase in MBH LHRH content. When prazosin was given every hour starting from the 10th to the 13th h after surgery, it was effective to prevent both the increase of MBH LHRH content and the decrease of serum LH found during sympathetic nerve degeneration. Similar repetitive injections of propranolol resulted in the greatest depression of serum LH, and in the greatest increase of MBH LHRH observed. Serum LH response to LHRH injection was similar in SCGx and sham-operated rats. The data indicate that SCG neurons exert, through inhibitory alpha 1-, and weaker, stimulatory beta-adrenoceptors, a significant influence on LHRH release at a supra-hypophysial site.

Failure of Naloxone to Stimulate Luteinizing Hormone Secretion during Pregnancy and Steroid Treatment of Ovariectomized Beef Cows1

The response of serum luteinizing hormone (LH) to naloxone, an opiate antagonist, and gonadotropin-releasing hormone (GnRH) was measured in cows in late pregnancy to assess opioid inhibition of LH. Blood samples were collected at 15-min intervals for 7 h. In a Latin Square arrangement, each cow (n = 6) received naloxone (0, 0.5, and 1.0 mg/kg BW, i.v.; 2 cows each) at Hour 2 on 3 consecutive days (9 +/- 2 days prepartum). GnRH (7 ng/kg body weight, i.v.) was administered at Hour 5 to all cows on each day. Mean serum LH concentrations (x +/- SE) before naloxone injection were similar (0.4 +/- 0.1 ng/ml), with no serum LH pulses observed during the experiment. Mean serum LH concentrations post-naloxone were similar (0.4 +/- 0.1 ng/ml) to concentrations pre-naloxone. Mean serum LH concentrations increased (p less than 0.05) following GnRH administration (7 ng/kg) and did not differ among cows receiving different dosages of naloxone (0 mg/kg, 1.44 +/- 0.20; 0.5 mg/kg, 1.0 +/- 0.1; 1.0 mg/kg, 0.9 +/- 0.1 ng/ml). In Experiment 2, LH response to naloxone and GnRH was measured in 12 ovariectomized cows on Day 19 of estrogen and progesterone treatment (5 micrograms/kg BW estrogen: 0.2 mg/kg BW progesterone) and on Days 7 and 14 after steroid treatment. On Day 19, naloxone failed to increase serum LH concentrations (Pre: 0.4 +/- 0.1; Post: 0.4 +/- 0.1 ng/ml) after 0, 0.5, or 1.0 mg/kg BW.(ABSTRACT TRUNCATED AT 250 WORDS)

Ovarian cyclicity and serum progesterone and luteinizing hormone in fine-wool ewes supplemented with alfalfa or pinto beans

Effects of season and supplementation on the incidence and rate of ovulation and hormone profiles in multiparous, nonlactating ewes were investigated under range and drylot conditions during anestrus (February through August). Ninety ewes received one of six nutritional treatments: 1) range forage, 2) range forage plus 0.33 kg·hd −1·d −1 pinto beans, 3) 0.45 kg·hd −1·d −1 alfalfa pellets, 4) dry lot plus 1.33 kg·hd −1·d −1 prairie hay only, 5) pinto beans or 6) alfalfa pellets at rates used on the range and prairie hay. Supplemented ewes were heavier (P < 0.05) than ewes fed range forage or prairie hay during most of the study. Seasonality of ovulation, in terms of incidence and rate, was not affected (P > 0.40) by supplementation in range ewes. The ovulation rate tended to be highest in prairie hay plus pinto bean drylot ewes in February (P = 0.21) and in prairie hay plus alfalfa pellet and prairie hay plus pinto bean ewes in March (P = 0.13) compared with prairie hay ewes. Generally, seasonality of ovulation was not influenced by supplementation (P > 0.40). The incidence of ovulation approached zero for drylot ewes in April, May, June and July, while it was 43, 27, 35 and 21% for range ewes, in those same months. Supplementation did not affect serum progesterone during the estrous cycle. Luteinizing hormone (LH) concentrations were similar (P > 0.50) among drylot treatment groups before a 50-ug gonadotropin releasing hormone (GnRH) challenge. Pinto bean supplementation enhanced serum LH response to GnRH (P < 0.10).

Isolated gonadotropin deficiency in boys: Clinical characteristics and growth

Analysis of the clinical findings and growth in 20 boys with isolated gonadotropin deficiency revealed a heterogeneous group of physical abnormalities. Ten of these patients were hyposmic or anosmic (Kallmann syndrome). Abnormalities found in our patients included undescended testes, gynecomastia, and ocular or skeletal anomalies. Regardless of the presence of hyposmia, patients without testicular enlargement (less than 2 cm3), had serum luteinizing hormone (LH) responses to luteinizing hormone-releasing factor (LRF) that were the same as in prepubertal boys. By contrast, five boys with testicular enlargement (greater than 2 cm3), some of whom had hyposmia, had a greater serum LH response to LRF than did prepubertal boys. Adrenarche was moderately delayed; although all boys initially had normal serum levels of dehydroepiandrosterone-sulfate, four boys eventually developed elevated serum levels. Bone ages were delayed compared with chronologic age in boys who had the condition after 15 years of age. The rate of linear growth was normal, and final adult heights were normal with testosterone therapy, although linear growth continued longer in these boys than in boys with normal pubertal progression. Although none of the patients was obese at the time of diagnosis, three patients developed obesity after initiation of testosterone therapy.

Testicular modulation of luteinizing hormone response to gonadotropin-releasing hormone (GnRH)-agonist treatment.

We and others have observed that the response of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) to chronic gonadotropin-releasing hormone-agonist (GnRH-A) treatment is substantially different in normal compared to hypogonadal males. These data suggested that products of the testes determine the gonadotropin response to GnRH-A. The present studies were designed to determine whether this effect is mediated by products of the interstitial (steroids) or the tubular compartment. To create experimental states with selective impairment of interstitial, tubular, or both compartments, 100 male sexually mature Wistar rats were divided into five groups: I, intact; II, castrated; III, castrated with 20-mm testosterone (T) implants; IV, bilaterally cryptorchid; and V, ketoconazole-treated animals. Cryptorchid animals have been shown to have impairment of tubular function while ketoconazole inhibits T biosynthesis. Each of the 5 groups was divided into 2 subgroups to receive daily injections of either saline or 1 microgram of a potent GnRH agonist, D-leu6 des-Gly10 GnRH N-ethylamide, for 4 wk. Unlike the intact animals, which showed an elevation of basal serum LH concentration after 4 wk of GnRH-A treatment, the castrated animals showed significant suppression below baseline. Animals with preferential impairment of tubular function (cryptorchid and castrated + T) also showed significant suppression of LH after GnRH-A treatment. However, the ketoconazole-treated animals (with inhibition of T biosynthesis and intact tubular function), behaved similarly to intact animals and demonstrated an elevation of LH after GnRH-A treatment.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of naloxone on serum luteinizing hormone, cortisol and prolactin concentrations in anestrous beef cows.

Two experiments were conducted with the opioid antagonist naloxone to determine the effect of opioid receptor blockade on hormone secretion in postpartum beef cows. In Exp. 1, nine anestrous postpartum beef cows were used to measure the effect of naloxone on serum luteinizing hormone (LH), cortisol and prolactin concentrations. Cows received either saline (n = 4) or 200 mg naloxone in saline (n = 5) iv. Blood samples were collected at 15-min intervals for 2 h before and after naloxone administration. Serum LH concentrations increased (P less than .01) in naloxone-treated cows from 1.8 +/- .04 ng/ml before treatment to 3.9 +/- .7 ng/ml and 4.2 +/- .5 ng/ml at 15 and 30 min, respectively, after naloxone administration. In contrast, LH remained unchanged in saline-treated cows (1.6 +/- .3 ng/ml). Serum cortisol and prolactin concentrations were not different between groups. In Exp. 2, 12 anestrous postpartum beef cows were used to examine the influence of days postpartum on the serum LH response to naloxone. Four cows each at 14 +/- 1.2, 28 +/- .3 and 42 +/- 1.5 d postpartum received 200 mg of naloxone in saline iv. Blood samples were taken as in the previous experiment. A second dose of naloxone was administered 2 h after the first, and blood samples were collected for a further 2 h. Serum LH concentrations increased (P less than .01) only in cows at 42 d postpartum.(ABSTRACT TRUNCATED AT 250 WORDS)

Seasonal reproduction in the mongoose, Herpestes auropunctatus: III. Regulation of gonadotropin secretion in the male

The seasonal regulation of gonadotropin secretion in the male mongoose was investigated by evaluating in vitro responsiveness of anterior pituitaries to gonadotropin releasing hormone (GnRH) and by evaluating postcastration gonadotropin responses in vitro and in vivo during the breeding and inactive seasons. The relative increase of luteinizing hormone (LH) from in vitro GnRH-stimulated anterior pituitaries was significantly greater during the active season than during the inactive season. The reduced responsiveness during the inactive season was related to an increase in the negative feedback actions of the testes at the hypophyseal level. In vitro follicle stimulating hormone (FSH) secretion from GnRH-treated anterior pituitaries was not significantly affected by season; however, a more potent negative feedback effect of the testes on basal FSH release was apparent during the inactive season. The postcastration serum LH response was more rapid during the active season than during the inactive season, whereas the postcastration serum FSH response was not affected by season.

Diurnal influences on serum luteinizing hormone responses to opiate receptor blockade with naloxone or to luteinizing hormone-releasing hormone in the immature female rat.

AbstractThe major objective of these studies was to determine whether there is a temporal pattern in the gonadotropin response of immature rats to luteinizing hormone-releasing hormone (LHRH) or the opiate antagonist, naloxone. Thirty-day-old female rats were injected at 3-hr intervals over a 24-hr period with either naloxone (2.5 mg/kg body wt) or LHRH (8 ng/100 g body wt). Animals were decapitated 15 min later and serum samples were assayed for luteinizing hormone (LH) by radioimmunoassay. The serum LH response to naloxone and LHRH varied significantly with the time of day. Naloxone administration had no statistically significant (P > 0.05) effect on levels of serum LH at 1500 and 1800 hr compared to levels in saline-injected controls, but induced a significant rise in serum LH at all other times. Naloxone had its greatest effect during the late evening and early morning hours (2100 to 0900 hr). A similar, but not identical, pattern of LH responsiveness to LHRH was observed, with the two rhythms being t...

Positive Feedback Effect of Progesterone on Luteinizing Hormone (LH) Release in Cyclic Female Rhesus Monkeys

The synergistic effects of progesterone (P) and estrogen on LH release were examined in nine monkeys with regular menstrual cycles. During six menstrual cycles, animals were subjected, in alternate cycles, to each of the following treatments in random order beginning at 0830 on the third day of the cycle: 1) 30 <g estradiol benzoate (EB) sc, 2) 30 jug EB sc, followed by 2.5 mg P sc 24 h later, or 3) 330 <g EB sc. During the seventh menstrual cycle, all animals were assigned again to either treatment 1 or 2. Blood samples were obtained at 3- to 24-h intervals, and serum concentrations of LH, estradiol, and P were determined by RIA. The high dose of EB induced the characteristic negative feedback response of serum LH, followed by the positive feedback response which peaked 36–54 h after EB, while the low dose of EB induced initial small decreases of LH within 24 h after EB, followed by slight increases of LH during the second and third days after EB. P administration after the low dose of EB induced two dis...

Positive Feedback Effect of Progesterone on Luteinizing Hormone (LH) Release in Cyclic Female Rhesus Monkeys: LH Response Occurs in Two Phases*

The synergistic effects of progesterone (P) and estrogen on LH release were examined in nine monkeys with regular menstrual cycles. During six menstrual cycles, animals were subjected, in alternate cycles, to each of the following treatments in random order beginning at 0830 on the third day of the cycle: 1) 30 <g estradiol benzoate (EB) sc, 2) 30 jug EB sc, followed by 2.5 mg P sc 24 h later, or 3) 330 <g EB sc. During the seventh menstrual cycle, all animals were assigned again to either treatment 1 or 2. Blood samples were obtained at 3- to 24-h intervals, and serum concentrations of LH, estradiol, and P were determined by RIA. The high dose of EB induced the characteristic negative feedback response of serum LH, followed by the positive feedback response which peaked 36–54 h after EB, while the low dose of EB induced initial small decreases of LH within 24 h after EB, followed by slight increases of LH during the second and third days after EB. P administration after the low dose of EB induced two dis...