Elevated Luteinizing Hormone Concentrations Research Articles

Progesterone receptor-Src kinase signaling pathway mediates neuroprogesterone induction of the luteinizing hormone surge in female rats.

Neural circuits in female rats are exposed to sequential estradiol and progesterone to regulate the release of luteinizing hormone (LH) and ultimately ovulation. Estradiol induces progesterone receptors (PGRs) in anteroventral periventricular nucleus (AVPV) kisspeptin neurons, and as estradiol reaches peak concentrations, neuroprogesterone (neuroP) synthesis is induced in hypothalamic astrocytes. This local neuroP signals to PGRs expressed in kisspeptin neurons to trigger the LH surge. We tested the hypothesis that neuroP-PGR signaling through Src family kinase (Src) underlies the LH surge. As observed in vitro, PGR and Src are co-expressed in AVPV neurons. Estradiol treatment increased the number of PGR immunopositive cells and PGR and Src colocalization. Furthermore, estradiol treatment increased the number of AVPV cells that had extranuclear PGR and Src in close proximity (<40nm). Infusion of the Src inhibitor (PP2) into the AVPV region of ovariectomized/adrenalectomized (ovx/adx) rats attenuated the LH surge in trunk blood collected 53h post-estradiol (50µg) injection that induced neuroP synthesis. Although PP2 reduced the LH surge in estradiol benzoate treated ovx/adx rats, activation of either AVPV PGR or Src in 2µg estradiol-primed animals significantly elevated LH concentrations compared to dimethyl sulfoxide infused rats. Finally, antagonism of either AVPV PGR or Src blocked the ability of PGR or Src activation to induce an LH surge in estradiol-primed ovx/adx rats. These results indicate that neuroP, which triggers the LH surge, signals through an extranuclear PGR-Src signaling pathway.

Elevated Pre-injection Basal Luteinizing Hormone Concentrations are Common in Girls Treated for Central Precocious Puberty

Objective:A consensus on how to monitor girls with central precocious puberty (CPP) during gonadotropin-releasing hormone agonist (GnRHa) treatment is lacking. Increased, unstimulated basal luteinizing hormone (LH) concentrations have been suggested to indicate lack of suppression. The aim was to evaluate pre-injection basal LH concentrations during GnRHa (leuprorelin 3.75 mg) treatment every four weeks in girls with CPP.Methods:Medical records were reviewed for girls with CPP treated at a single center from 2014-2019. Clinical characteristics and laboratory findings during treatment were systematically recorded.Results:A total of 587 GnRHa pre-injection basal LH concentrations were analyzed in 74 girls. Basal LH was pubertal (≥0.3 IU/L) in 53.5% of blood samples and 87.8% of all girls had a pubertal basal LH concentration at least once. A GnRH test (n=29) was repeated in 23 girls due to suspicion of clinical progression, elevated basal LH or recordable estradiol concentrations. None had a stimulated LH >3.1 IU/L. The predictability of treatment suppression (specificity) of basal LH concentrations was 12.0% when compared to repeated GnRH stimulation tests. Despite shortening the GnRHa injection interval to three weeks, basal LH concentrations remained pubertal in 85.7% girls. A significant reduction in height standard deviation score (p<0.001) and bone age advance (p<0.001) was observed during treatment.Conclusion:Pre-injection basal LH remains at pubertal concentrations during treatment with leuprorelin 3.75 mg in girls with CPP. Clinical monitoring of pubertal progression is preferable to routine basal LH concentrations. Repeat GnRH stimulation testing should be regarded as the gold standard.

Expression of LHCG receptors in the human penis

The aim of this study is to investigate the expression of the luteinizing hormone/choriogonadotropin (LHCG) receptor in the human penis to see, if the luteinizing hormone (LH) effects are possible in the spongious and cavernous tissue of the penis. The number of men with erection disturbances increases significantly simultaneously with the elevated LH concentrations between 40 and 70 years. It is possible that the elevated LH concentrations may influence locally the erectile mechanisms. The precondition for this is the expression of LHCG receptors in the penis. Penile tissue was obtained from three patients undergoing total or partial penectomy due to a rectal cancer with secondary penile metastasis or squamous cell carcinoma of the penis. Immunohistochemistry was used for the detection of the LHCG receptor. Positive immunoreaction for LHCG receptors was discovered in the endothelial cells of cavernous spaces in the corpus cavernosum and corpus spongiosum penis, also in the endothelial cells of the capillary walls in all patients. Our results show that LHCG receptor is expressed in the spongious and cavernous tissue of the human penis. This finding suggests that LH can affect the spongious and cavernous tissue in human and play a significant role in the development of erectile dysfunction among the aging men.

Pregnancy complications in PCOS

Complications of pregnancy associated with maternal PCOS include increased prevalence of early pregnancy loss (EPL), gestational diabetes (GDM), pregnancy-induced hypertensive disorders (PET/PIH), and the birth of small-for-gestational-age (SGA) babies. Increased risk of EPL has been attributed to obesity, hyperinsulinaemia, elevated luteinizing hormone concentrations, and endometrial dysfunction. Avoiding obesity before pregnancy and treatment with metformin are therapeutic options, also for the increased prevalence of GDM. Administration of metformin throughout pregnancy is a contentious issue. Screening pregnant women with PCOS for GDM and PET/PIH-especially if they are obese-is recommended, although data for a firm association between PCOS and PET/PIH is weak. Impaired insulin-mediated growth and fetal programming are possible explanations for a higher prevalence of SGA infants in mothers with PCOS. Only prospective studies employing a large cohort of women with well-defined PCOS compared with a control group matched for BMI and parity can solve the remaining questions.

Pituitary content of luteinizing hormone reveals species differences in the reproductive synchrony between males and females in Australian flying-foxes (genus Pteropus).

Flying-foxes (genus suborder, Pteropus Megachiroptera) are long-lived tropical mammals. Their seasonal reproduction appears to be regulated by an endogenous, circannual rhythm modified by multiple environmental cues. Luteinizing hormone (LH) content in pituitary extracts was examined to establish the broad time-frame of pituitary stages in the reproductive seasonality of the flying-foxes. A comparison was made between the grey-headed flying-fox P. poliocephalus, which mates and conceives in autumn, and the little red flying-fox P. scapulatus, which mates and conceives in spring. In P. scapulatus, LH was maximum during the spring mating season at 1494 ng mg(-1) in males and 896 ng mg(-1) in females. In P. poliocephalus males, LH increased to 1082 ng mg(-1) in early summer, 4 months before the mating season; LH concentrations in male P. poliocephalus returned to a low of 222 ng mg(-1) by the time of the autumn mating, by which time the female P. poliocephalus expressed elevated LH concentrations (624 ng mg(-1)). Apparently in P. poliocephalus, the peak LH concentrations in females are delayed by 4 months relative to LH concentrations in males. This is associated with 4 months of energetic courtship on the part of male P. poliocephalus, which is not observed in P. scapulatus, the fertility of which is synchronized between the sexes. The heterologous radioimmunoassay developed using monoclonal antibody 518B7 confirmed classic suppression of LH during pregnancy and lactation in flying-foxes and LH elevation in response to gonadectomy. Juveniles generally had pituitary levels similar to non-breeding levels in adults.

Semen parameters and hormone concentrations in stallions subjected to long-term estrogen administration

Eight pony stallions were paired by estimated daily sperm output (DSO) and randomly assigned to one of two treatments in a randomized block experiment. Stallions received 44 μg/kg BW estradiol cypionate (ECP) or an equivalent volume of physiological saline solution on alternate days during the breeding season. Blood samples collected immediately preceding each injection were assayed for luteinizing hormone (LH), estradiol-17β (E2) and testosterone (T). Semen was collected twice weekly, 3.5 days apart, to evaluate sperm motility and total number of sperm per ejaculate. Prior to and after 4, 8 and 12 weeks on treatment, semen was collected once daily for 7 days to determine DSO. Data were separated into 9 periods (10 days each) for statistical analysis and subjected to analysis of variance for a randomized block design to determine treatment effects. There were no differences (p>.05) between groups for DSO or LH prior to initiation of treatment. Testosterone was higher (p<.05) in ECP stallions compared with C stallions prior to treatment and at all time points measured. As expected, E2 was higher (p<.05) in the ECP stallions compared to C stallions after 20 days (period 2) of treatment and for the remainder of the experiment. However, E2 was higher (p<.05) in the C group prior to treatment, but there was no difference between the groups after 10 d of treatment (period 1). ECP stallions had higher (p<.05) DSO than C stallions after 30 d on treatment. After 40 and 50 d (periods 4 and 5), ECP stallions demonstrated higher (p<.05) total sperm per period than C stallions. This was preceded by higher (p<.05) LH values for ECP stallions than for C stallions after 10 and 20 d (periods 1 and 2). No differences were found between the ECP and C groups for LH between 30 and 60 d. Although numerically higher, no significant differences (p>.05) were seen after 60 days for DSO or after 60, 70 or 80 days for total sperm per period. ECP stallions had higher (p<.05) DSO and total sperm per period after 90 d than C stallions. Additionally, LH remained significantly higher (p<.05) in the ECP group after 60 days (periods 7, 8 and 9). Elevated LH concentrations in ECP stallions demonstrated that estrogen treatment did not inhibit LH secretion in this study.

Pregnancy outcome following exposure to gonadotrophin-releasing hormone analogue during early pregnancy: comparisons in patients with normal or elevated luteinizing hormone

The outcomes of established pregnancies following the treatment of infertile women with pituitary down-regulation before and during treatment with ovulation induction and either intrauterine insemination or timed intercourse were reviewed. Once started on gonadotrophin-releasing hormone analogue (GnRHa) treatment, the patients were maintained on GnRHa therapy throughout the following luteal phase to facilitate the start of the next treatment cycle if no pregnancy was established. This resulted in patients taking GnRHa until a positive pregnancy test indicated cessation of the treatment. The aim of our study was to determine whether exposure to GnRHa during early pregnancy constituted a risk. Patients who were diagnosed as having elevated follicular phase luteinizing hormone (LH) concentrations during their investigations were analysed as a separate cohort to assess whether this diagnosis had implications with respect to pregnancy outcome. Out of 226 recorded clinical pregnancies, 173 were traced and the data collated: 16 cases resulted in clinical abortions, two were ectopic pregnancies and 155 women had live births at various ages of gestation. There were three pregnancies which were complicated by congenital abnormalities. Patients with elevated LH concentrations on examination showed a higher rate of total pregnancy loss than those with normal LH concentrations, despite the fact that the LH was suppressed during the cycle in which they conceived. The results suggest that pregnancy outcome is not adversely affected by GnRHa administration during the luteal phase of the conception cycle, and that the group diagnosed as having elevated LH concentrations may retain their propensity to higher rates of pregnancy loss even when their LH concentrations are suppressed during treatment.

Menopause in female rhesus monkeys.

Fifteen female rhesus monkeys (Macaca mulatto), ranging in age from 8 to 34 years, were studied for one year to characterize the endocrine and menstrual changes associated with menopause in this species. Five monkeys were premenopausal; these younger monkeys, ages 8-11 years, menstruated and showed cyclic ovarian activity during the 12-month study period, as evidenced by menses and periodic elevations of serum estradiol (E2) and luteinizing hormone (LH) concentrations. Four females, ages 24-26 years, were in transition to menopause. Two of these perimenopausal females menstruated and secreted E2 and LH in a periodic fashion; the other two females showed elevated LH concentrations, consistently low E2 levels, and no evidence of menstruation. Six females, ages 27-34 years, were clearly postmenopausal; LH concentrations were high, whereas E2 concentrations were uniformly low. There was a significant inverse correlation between basal E2 concentrations and age, and a significant positive correlation between age and LH concentrations across all 15 animals. Hormonal changes indicative of ovulation, when they occurred, were generally restricted to the winter and early spring months. Histological analysis of ovaries from four postmenopausal females revealed little or no evidence of active folliculogenesis. These data indicate that menopause in female rhesus monkeys does not occur until the second half of thethird decade of life. © 1995 Wiley-Liss, Inc.

Serum progesterone and luteinizing hormone in ewes treated with PGF 2α during mid-gestation and gonadotropin releasing hormone after parturition

Two studies were conducted to determine if postpartum (PP) reproductive function could be enhanced in ewes by PGF 2α during mid-gestation (Trial 1) and GnRH within 10 days PP (Trial 2). Trial 1 utilized 31 ewes (x̄ body weight = 84 kg) assigned to two treatment groups to receive (I.M.) either saline (control, n = 17) or PGF 2α (0.14 mg/kg body weight, n = 14) on day 74 of gestation. Results from the first study indicated success in regressing the corpus luteum (CL) of pregnancy as indicated by decreased serum progesterone (P 4, P < 0.05) by 24 hours after treatment. In addition, by 20 days after treatment, serum luteinizing hormone (LH) concentrations in treated ewes were higher ( P < 0.01) than in controls. However, ovarian activity was not re-established by 30 days PP in this study. In Trial 2, 35 ewes (x̄ body weight = 79 kg) were randomly assigned to one of four groups: no treatment (controls, n = 9), PGF 2α (no GnRH, n = 9), GnRH (no PGF 2α n = 9) or both PGF 2α and GnRH (n = 9). The PGF 2α-treated animals received 0.14 mg PGF 2α/kg body weight (I.M.) on day 73 of gestation and GnRH-treated ewes received 50 μg GnRH (I.M.) on days 2, 6, and 10 PP. As in Trial 1, P 4 concentrations in PGF 2α-treated ewes were lower ( P < 0.02) than in control ewes by 24 hours after treatment. Progesterone remained lower in PGF 2α-treated animals through day 116 of gestation. However, no differences were detected ( P > 0.65) in LH concentrations between the two groups in this same period. Likewise, no differences were observed ( P > 0.32) in LH concentrations between the PGF 2α-treated and control ewes on days 2, 6, and 10 PP. However, elevated ( P < 0.07) LH concentrations were noted in ewes receiving 50 μg GnRH compared with ewes not receiving GnRH. In addition, area under the LH curve (AUC) was greater ( P < 0.01) for GnRH-treated animals on days 2, 6, and 10 PP and LH AUC increased over the PP period in GnRH-treated ewes. Three of eight ewes receiving both PGF 2α and GnRH treatments had ovarian activity within 30 days PP as indicated by P 4 concentrations above 1 ng/ml while no other ewes had ovarian activity during this time period.

Failure of the gonadotropin-releasing hormone stimulation test to detect inadequate response to leuprolide treatment in central precocious puberty

In two girls with central precocious puberty, inadequate clinical response to daily leuprolide treatment was associated with suppressed radioimmunoassayable luteinizing hormone (LH) levels to gonadotropin-releasing hormone (GnRH) stimulation. Elevated serum LH concentrations were, however, demonstrated by a highly sensitive immunoradiometric assay. Thus, traditional radioimmunoassays for LH may be inadequate to monitor response to GnRH agonist treatment, even when they are used in combination with a GnRH stimulation test.

Hypogonadism Caused by a Single Amino Acid Substitution in the β Subunit of Luteinizing Hormone

WEISS, JEFFREY; AXELROD, LLOYD; WHITCOMB, RANDALL W.; HARRIS, PHILIP E.; CROWLEY, WILLIAM F.; JAMESON, J. LARRY Author Information

Hypogonadism Caused by a Single Amino Acid Substitution in the β Subunit of Luteinizing Hormone

INFERTILITY occurs in approximately 10 to 20 percent of couples and can be attributed to a reproductive disorder in the man or woman with equal frequency.1 , 2 Among men, specific causes of infertility can be identified in only a minority.1 In a previously identified kindred in which several men were infertile, the proband had not undergone spontaneous puberty and had low testosterone and elevated luteinizing hormone concentrations in serum, a pattern of hormone values indicative of primary hypogonadism.3 However, testosterone secretion in response to the administration of exogenous luteinizing hormone and human chorionic gonadotropin was normal. Thus, the proband appeared to . . .

Development of an endocrine challenge test to investigate subfertility in ewes

Simultaneous or sequential injection of 250 ng gonadotrophin releasing hormone (GnRH) and 25 μg oestradiol benzoate, with luteinizing hormone (LH) measurements at 0, +20 min (after GnRH) and +16 h (after oestradiol), enabled investigation of the positive feedback effects on the hypothalamus and pituitary. Control ewes had pretreatment LH values of 3·1 ± 1·2 ng/ml with an increment of 3·2 ± 2·3 ng/ml 20 min after GnRH. Subfertile ewes, in spite of elevated pretreatment LH concentrations (15·8 ± 9·5 ng/ml) in eight out of 10 ewes, had increments of 1·4–84 ng/ml after GnRH. Control ewes had LH increments of 3–75 ng/ml 16 h after oestradiol. Subfertile ewes with pretreatment LH concentrations < 15 ng/ml also responded to oestradiol whereas those with initial LH concentrations 16–40 ng/ml had no further LH increment. Subsequent administration of 1000 iu pregnant mares' serum gonadotrophin (PMSG), with measurement of LH and oestradiol at 0, +24, +30, +48, +54, and +72 h, allowed assessment of ovarian response and hypothalamus-pituitary function. Five control ewes were sampled up to 30 h post-PMSG and only 1 had oestradiol concentrations > 10 pg/ml. Sampling up to 72 h in another five control ewes resulted in oestradiol concentrations > 10 pg/ml. Increments in LH concentration > 3 ng/ml were recorded in control and subfertile ewes with oestradiol concentrations > 10 pg/ml. The use of these endocrine challenge tests enabled positive diagnosis of abnormality on 8 out of 10 occasions. Post-mortem examination of seven of the subfertile ewes revealed reproductive tract abnormalities characterized by very small inactive ovaries, and in four cases complete absence of oviducts, uterus, cervix and anterior vagina (although these latter abnormalities could not have been diagnosed from the tests described).

Suppression of spontaneous LH surges in estrogen-treated ovariectomized rats by microimplants of antiestrogens into the preoptic brain

Studies by others have shown that parenteral administration of antiestrogens blocks the positive feedback effect of estrogen on the luteinizing hormone (LH) surge mechanism. Since all estrogen-accumulating cells could be affected by this treatment, it is difficult to identify the site(s) at which this steroid acts to affect LH surges. In the present study we attempted to deprive specific hypothalamic neurons of estrogen by stereotaxically implanting antiestrogen-containing microcannulae into the brains of ovariectomized (OVX) rats which, otherwise, were completely estrogenized. The animal model used in these studies was the 14-day OVX rat into which 2 estradiol-containing Silastic capsules were inserted s.c. on day 14 (day 0). Microcannulae were placed into either the medial or lateral preoptic nuclei (MPN, LPN) on day 0 and the effects on LH release were examined 2 days later (day 2). When empty cannulae were placed into the MPN or LPN, 6 of 7 and 8 of 8 rats, respectively, had normal spontaneous LH surges. In contrast, when cannulae containing either CI-628, LY 10074 or Keoxifene were implanted into MPN only 33.3, 0, and 14.3% of the rats, respectively, had LH surges by 16.00 h on day 2 (time of LH peak). When antiestrogen-containing cannulae were placed into the LPN, all rats displayed normal LH patterns of release and concentrations. The antiestrogens did not prevent estrogen from suppressing elevated high post-ovariectomy plasma LH concentrations (negative feedback). To evaluate whether Keoxifene affected releasable luteinizing hormone-releasing hormone (LH-RH), we examined the effects of MPN-Keoxifene implants on LH sercretion evoked by electrochemical stimulation (ECS) of the MPN or the medial basal hypothalamus (MBH). In ketamine-anesthetized rats with empty cannulae, plasma LH increase significantly to reach peak concentrations 30–45 min after ECS. Similar LH concentrations and release patterns occurred in rats with the antiestrogen implant. Other studies examined the effects of MPN-Keoxifene implants on norepinephrine (NE) concentrations and rate constants following administration of α-methyl- p-tyrosine. NE concentrations and rate constants in the MPN and median eminence did not differ significantly in rats which had received empty versus Keoxifene-containing microcannulae. In the final series of studies we examined the response of LH-RH neurons to an intracerebroventricular (i.c.v.) infusion of norepinephrine (20 μg). Plasma LH peaked within 10 min after i.c.v. NE and, thereafter, declined towards baseline. Keoxifene did not affect LH-RH neuronal responsiveness to i.c.v. NE. Thus, while each of the antiestrogens studied had profound effects on spontaneous LH surges, the mechanism(s) by which these drugs exerted their effect remains unresolved. Releasable LH-RH pools were not altered and neither NE turnover rates in the MPN or median eminence nor LH-RH neuronal responsiveness to NE was affected. However, it is possible that transduction of the endogenous NE signal required for the LH surge may be affected by alterations in the activity of estrogen-containing interneurons when antiestrogens are placed in the vicinity of LH-RH perikarya.

Plasma LH and gonadal LH-binding cells in normal and surgically decapitated chick embryos

Plasma luteinizing hormone (LH) concentrations and the numerical density ( N v) of gonadal LH-binding (LH-positive) cells were determined in intact male and female chick embryos from Days 10.5 through 18.5 of incubation for plasma LH and from Days 6.5 through 19.5 for LH-binding cells, as well as in Day 15.5 decapitated (“hypophysectomized”) embryos with pituitary transplants for both plasma LH and LH-binding cells. The data demonstrate that LH is already present in the plasma of male and female embryos as early as Day 10.5, the first day examined. Plasma LH levels in hypophysectomized embryos were statistically significantly lower than those of intact embryos, while pituitary transplants to the chorioallantoic membrane of hypophysectomized embryos elevated plasma LH concentrations to levels not statistically different from those of intacts. The “role(s)” of plasma LH levels and changes in form and numerical density ( N v) of gonadal LH-binding cells in the maturation of the pituitary-gonadal axes of the chick embryo are discussed and evaluated.

Elevated plasma luteinizing hormone concentrations, cryptorchidism and mania

A young man with acute mania and unilateral cryptorchidism had plasma luteinizing hormone (LH) concentrations that were much higher than the maximum LH concentrations we have found in normal subjects and patients with schizophrenia. Plasma concentrations of testosterone and sex hormone binding globulin were not abnormal, showing that the elevated plasma LH concentrations were probably due to increased secretion of LH-releasing hormone (LHRH). This case supports our previous results which suggest that an abnormally high secretion of LHRH, due presumably to an abnormality in central neurotransmission, may be a feature of acute mania in young men.

Hypergonadotropism in Peripubertal Boys with Chronic Renal Failure

Serum gonadotropin and testosterone concentrations were measured in ten peripubertal boys to assess the effects of uremia on pubertal maturation. Serum luteinizing hormone (LH) concentrations were elevated for stage of puberty in eight boys, whereas in most boys serum follicle-stimulating hormone and testosterone concentrations were normal. Serum LH concentrations correlated with the severity of uremia. LH levels declined when measured 1 year after the initial measurements in four boys who received renal allografts, but were further elevated in two boys who were treated conservatively. Elevated serum LH concentrations in the presence of normal serum testosterone concentrations imply limited testicular sensitivity to the effects of LH in these peripubertal boys, as has been documented for adult men with chronic renal failure. Alternatively, there may be accumulation of an immunoreactive LH molecule that lacks bioactivity. A testicular dysfunction may explain the pubertal delay experienced by some uremic adolescent boys.

Abnormalities of the Hypothalamic—Pituitary—Leydig Cell Axis in Young Adult Rats with Vitamin A Deficiency

The hypothalamic concentration of gonadotrophin releasing hormone (GnRH), the in vivo pituitary responses to GnRH, and the in vivo Leydig cell responses to bovine luteinizing hormone (LH) and to endogenous LH were determined in young adult male rats who had been on a vitamin‐A‐deficient (VAD) diet for 64 days and in age‐matched controls. Hypothalamic GnRH content was 3.06 ± 0.25 ng/hypothalamus in VAD (mean ± SEM) and 3.26 ± 0.25 ng/hypothalamus in controls. Baseline serum LH concentrations were 24.6 ± 4.7 ng/ml in VAD and 11.3 ± 2.3 ng/ml in controls (P &lt; 0.02). Baseline serum follicle stimulating hormone (FSH) levels were 373 ± 61 ng/ml in VAD and 329 ± 16 ng/ml in controls. Fifteen minutes after administration of GnRH serum LH was 215 ± 16.3 ng/ml in VAD vs. 148 ± 18.3 ng/ml in controls (P &lt;0.02). Serum FSH levels 15 minutes after administration of GnRH were 866 ± 67 ng/ml in VAD vs. 566 ± 58 ng/ml in controls (P &lt; 0.01). Baseline serum testosterone (T) concentratio̊nswere 1.0 ± 0.2 ng/ml vs. 1.7 ± 0.3 ng/ml in controls (n.s.). Sixty minutes after exogenous LH administration, serum T concentrations were 21.7 ± 1.0 ng/ml in VAD vs. 17.8 ± 1.0 ng/ml in controls (P &lt;0.05). Sixty minutes after administration of GnRH, which elevated endogenous LH serum concentrations, serum T concentrations were similar in both groups (7.8 ± 0.9 ng/ml for VAD vs. 9.7 ± 0.5 ng/ml for controls). The elevated serum LH concentrations, together with the increased pituitary responses to GnRH, are compatible with an appropriate hypothalamic‐pituitary response to a direct impairment in testicular function secondary to the VAD. However, the increased in vivo Leydig cell responses to exogenous LH stimulation in these young adult males with VAD remains unexplained.

Postcoital Luteinizing Hormone Release in Male and Female Rabbits as Determined by Radioimmunoassay

We have developed a homologous radioimmunoassay for rabbit luteinizing hormone (LH), which was used to measure LH levels in sera of male and female rabbits before and after copulation. The results demonstrated the following: (1) LH concentrations in male and estrogen-primed female rabbits are similar prior to coitus; (2) following coitus, LH levels rise within 3 minutes in both sexes and reach a peak or plateau within 15 minutes; (3) elevated LH concentrations are maintained at a plateau for at least 1 hour in females and then fall toward base line values; (4) an increase in serum LH to 300 ng/ml (10- to 11-fold) or greater is sufficient to cause ovulation and the formation of corpora lutea; and (5) the postcoital rise in LH levels is greater in estrogen-primed females than in nontreated males.

Effects of ovariectomy and season on plasma luteinizing hormone in mares.

Six pony mares were ovariectomized (OVX) on day 16 of diestrus during June and July, 1972, to study short term changes in plasma luteinizing hormone (LH) concentrations. Plasma LH was higher (P less than .05) 3 days after OVX (1.76 ng/ml) than the day after OVX (1.01 ng/ml), and a gradual increase occurred over the first 2 weeks. Elevated plasma LH concentrations similar to mid-estrus levels were present from the 2nd to 11th week post-OVX. In another experiment, the same 6 OVX mares were bled once a month from February, 1973, to January, 1974, to study long-term changes in plasma LH in relation to the anestrous (November-April) and breeding seasons (May-October). Mean monthly plasma LH concentrations in OVX mares during all months of the anestrous season were lower (P less than .05) than mean monthly plasma LH during the months of June-September of the breeding season. During the transition from anestrous to breeding seasons (April, May) and breeding to anestrous seasons October, November), mean plasma LH concentrations were not significantly different between April and May (1.39 vs 1.84 ng/ml) and between October and November (3.02 vs 2.56 ng/ml), but April and May levels were lower (P less than .05) than October and November levels. Mean monthly plasma LH levels in OVX mares during the anestrous season were similar to those in intact mares during the anestrous season and at mid-diestrus during the breeding season. Mean monthly plasma LH levels in OVX mares during the breeding season were similar to plasma LH levels at mild-estrus in intact mares. These data indicate the presence of inhibitory (most likely progesterone) and stimulatory (most likely estrogen) influences from the ovary which modulate the endogenous LH pattern in mares during the breeding season.