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PubMed1989

Responses of luteinizing hormone (LH) and follicle-stimulating hormone levels to exogenous gonadotropin-releasing hormone during the estrogen-induced LH surge in the ovariectomized rhesus monkey.

Experiments were performed to study the responsiveness of the pituitary to gonadotropin-releasing hormone (GnRH) during the dynamic changes in gonadotropin secretion associated with the estrogen-induced luteinizing hormone (LH) surge in the ovariectomized (OVX) rhesus monkey. Silastic capsules filled with estradiol-17-beta were implanted subcutaneously in ovariectomized rhesus monkeys, resulting in an initial lowering of circulating LH and follicle-stimulating hormone (FSH) concentrations followed by an LH-FSH surge. GnRH was injected intravenously just before estrogen implantation, during the negative feedback response and during the rising, the peak, and the declining phases of the LH surge. The LH and FSH responses during the negative feedback phase were as large as those before estrogen treatment (control responses). During the rising phase of the LH surge, the acute response to GnRH injection did not differ significantly from the control response, but the responses 60 and 120 min after injection were somewhat increased. During the declining phase of the LH surge, the pituitary was not responsive to exogenous GnRH, although LH probably continued to be secreted at this time since the LH surge decreased more slowly than predicted by the normal rate of disappearance of LH in the monkey. We conclude that an increased duration of response to GnRH may be an important part of the mechanism by which estrogen induces the LH surge, but we do not see evidence of increased sensitivity of the pituitary to GnRH as an acute releasing factor at that time.

Animals↗
PubMed1976

Dissociation between LH release and pituitary cyclic nucleotide accumulation in response to synthetic LH-releasing hormone in vivo.

In order to clarify the role of cyclic nucleotides in the mediation of LH-releasing hormone (LH-RH) action on LH release, the effect of LH-RH on LH release and pituitary cyclic AMP and cyclic GMP accumulation was studied in vivo. Pituitary cyclic AMP levels were increased 10 min after the intraveneous injection of 2 mg dibutyryl cyclic AMP (db-cyclic AMP) or 25 mg aminophylline. However, serum LH levels were not altered at 10, 30 or 60 min after the administration of either agent. Synthetic LH-RH (100 ng/rat) increased serum LH levels as measured 10 min after injection, but no effect on either pituitary cyclic AMP or cyclic GMP was seen 1, 5 or 10 min after LH-RH administration. These in vivo results are contradictory to the second messenger hypothesis for either cyclic AMP or cyclic GMP in the mediation of LH-RH-induced LH released and suggest that further work must be done in order to confirm or reject this hypothesis.

Aminophylline↗
PubMed1976

Synthesis of LH-RH by rat hypothalamic tissue in vitro: I. Use of a specific antibody to LH-RH for immunoprecipitation.

Following the procedure of Jeffcoate et al. [1974] we have successfully obtained a specific antiserum to LH-RH in rabbits, and are utilizing our antibody to study the synthesis of LH-RH by rat hypothalamic tissues in vitro. Our antibody, used at a dilution of 1:20,000, binds 37% of added 125I-labelled LH-RH, and cross-reacts minimally with thyrotropin releasing factor (TRF; 4.0%), somatotropin release inhibiting factor (SRIF; 0.035%), and melanocyte inhibiting factor (MIF; 0.009%). The antiserum recovers LH-RH added to charcoal-stripped rat serum quantitatively. Serial dilutions of rat hypothalamic extract and varying aliquots of normal rat serum are parallel to the standard curve (synthetic LH-RH: 0-100 pg/tube). Hypothalamic tissue of 4 male rats, bounded by the optic chiasm, mammillary bodies and hypothalamic fissures to a depth of 2-3 mm, was pooled, minced and incubated for 1-3 h in 2 ml of Eagle's Minimum Essential Medium in atmosphere of 95% O2/5% CO2 with 10 muCi of 3H-glycine. Reactions were stopped by the addition of 1 ml 0.1 N HC1. The tissue and medium were homogenized together and boiled for 3 min. Aliquots from the incubates were neutralized, LH-RH levels measured by radioimmunoassay (RIA), and 3H-glycine incorporation determined by immunoprecipitation, using our antibody. 3H-glycine incorporation into presumptive LH-RH increased linearly over the 3 h period. Aliquots of the 3 h incubates were chromatographed on Sephadex G-25 columns (1 x 10 cm) using 0.01 M acetic acid for elution; 1 ml fractions were collected. Synthetic LH-RH was chromatographed in a similar manner, and its elution profile determined by UV absorbance at 280 mm. Aliquots of each fraction of the eluted material from the 3 h incubates were counted in a scintillation counter to determine the elution pattern of the labelled material. Additionally, aliquots from the 1 ml fractions were neutralized and used for immunoprecipitation. Coincident peaks of 3H-label, immunoprecipitable 3H-labelled presumptive LH-RH, and synthetic LH-RH were observed. These results lend strong evidence to support our conclusion that the technique of immunoprecipitation is an efficacious approach to the study of the synthesis of LH-RH by rat hypothalamic tissue in vitro.

Animals↗
PubMed1986

Short-term pituitary desensitization to LH-RH after pulsatile LH-RH in the ovariectomized rat: an in vivo experiment.

The development of acute insensitivity of pituitary LH secretion to LH-RH after a short exposure to LH-RH is described. In the first experiment, ovariectomized (OVX), phenobarbital-pretreated rats were given pulses of LH-RH (1.25 or 6.25 ng/100 g body weight (b.w.), intravenously). In rats given 1.25 ng at time 0, 6.25 ng at 60 min, 1.25 ng at 80 min and 1.25 ng at 120 min, there was a substantial increase in plasma LH after the first two injections, no increase after the third injection and a relatively small increase after the fourth one. In other rats treated identically but not given a 1.25-ng dose at 80 min, the plasma LH rise in response to the 1.25-ng dose at 120 min was comparable to that seen after the 1.25-ng dose given at time 0. If the 1.25-ng LH-RH pulses given at times 0 and 80 min were replaced by a rat pituitary extract, the plasma LH rise in response to the 1.25-ng dose at 120 min was comparable to that seen after administration of pituitary extract. In the second experiment, OVX phenobarbital-pretreated rats were given 1.25 ng LH-RH/100 g b.w. at t = 0. They were then divided into three groups, each receiving 1.25, 3.75 or 6.25 ng LH-RH/100 g b.w. at t = 60 min. Each of these three groups was again divided into three groups which received 1.25 ng LH-RH/100 g b.w. at 80, 100 or 120 min.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Radioimmunologic assessment of the level of circulating LH antibodies after passive immunization of the rat: relation to the level of LH secretion.

A double antibody radioimmunologic technique was used to estimate circulating levels of "free" LH antibodies (Ab) (i.e., Ab available for binding to radioiodinated rat LH in vitro) after a single injection of an equine antiserum to bovine LH (LH-AS) into cyclic (diestrus-1), early pregnant (d 6 or d 8), short-term (1 d) or long-term (12 d) ovariectomized, or 8-d hypophysectomized female rats. In both cyclic and pregnant rats given 0.5 ml LH-AS sc the blood Ab levles peaked 1 to 2 days after injection and then decreased exponentially (half-time: 14.6-17.0 h) and equally: vaginal estrus also appeared in the cyclic and the aborting pregnant rats on the 6th day, and ovulation on the 7th day after LH-AS treatment, when the blood levels had fallen to very low values. The rate of exponential decrease in blood Ab levels was not affected by other routes of administration (iv or ip) of LH-AS, or by sc doses of 1.0 or 0.25 ml, although the peak levels and their duration were related to dose and route of administration. Ovariectomy significantly increased the rate of exponential Ab decrease (half-time: 9.8 h in rats tested 12 days after operation) and hypophysectomy markedly diminished it (half-time: 63.0 h in rats tested 8 days after operation). Daily treatment of hypophysectomized rats with 20 mu/day of ovine LH from the time of LH-AS injection increased the rate of exponential Ab decrease to one approaching that of the intact rats (half-time: 20.5 h). Free LH antibodies thus seem to disappear from the circulation at a rate proportional to the amount of LH in the circulation.

Animals↗
PubMed1976

Simulation of the proestrous luteinizing hormone (LH) surge after infusion of LH-releasing hormone in phenobarbital-blocked rats.

Four-day cycling rats were kept in a room with the lights on from 0500-1900 h. Injection of an ovulation-blocking dose of phenobarbital at 1230 h on proestrus did not alter the rise in plasma LH concentration in response to rapid injection of 12.4, 124, or 1240 ng of LHRH at 1300 h. In additional blocked rats, blood was rapidly withdrawen through one of two indwelling atrial cannulas while LHRH was infused at a constant rate through the other. Administration of a given amount of LHRH by slow infusion was much more effective in elevating plasma LH than was rapid injection of the same amount of releasing hormone. The pattern of plasma LH concentration after infusion of approximately 50 ng of LHRH per hour from 1500-1810 h was remarkably similar to that of the spontaneous LH surge, i.e., a gradual rise in plasma LH concentration followed by a steep linear increase to high levels which remained elevated for a period of approximately 2 h before declining rapidly soon after the end of infusion. In rats given a second 3 h infusion of LHRH at the same rate, from 2200 to 0100 h, a different response pattern was seen: the initial increase in plasma LH was greater, but the linear rise, which ensued after a lag period of similar duration (about 45 min), was less marked. Prolongation of the first infusion beyond 1800 h did not prolong the plateau: plasma LH levels declined before the infusion was terminated. This decline was less rapid than that seen at the end of a spontaneous LH surge, which in turn was less rapid than that seen after termination of a 3 h and 10 min infusion starting at the same time (1500 h), suggesting that both LHRH release and pituitary responsiveness are diminished (but not abolished) at this time. These findings clearly indicate that, in phenobarbital-blocked proestrous rats, the major part of the proestrous LH surge (including rising and plateau phases) can be simulated by a constant-rate infusion of about 150 ng of LHRH over the 3 h and 10 min period beginning at 1500 h. Since the data also suggest that LHRH release is reduced and/or occurs sporadically during the terminal phase of the surge (when plasma LH levels are declining), these experiments imply that the LH surge is caused by a properly timed, nearly constant-rate release of LHRH for about 3 h (beginning about 1500 h of proestrus) followed by a period of diminished LHRH release.

Animals↗
PubMed1976

Luteal cell receptor content for prolactin (PRL) and luteinizing hormone (LH): regulation by LH and PRL.

The effect of LH and PRL during the differentiation of granulosa cells to luteal cells was examined by determining the ability of LH and PRL to regulate luteal cell receptor content for these hormones and to increase production of progesterone. Preovulatory follicles and corpora lutea were hormonally induced in immature hypophysectomized female rats by sequential treatment with estradiol, hFSH and oLH. The content of receptor for LH was high in granulosa cells of large antral follicles. Administration of LH caused receptor for LH to decrease markedly within 24 h and to remain low for 96 h. In contrast, granulosa cell content of receptor for PRL increased progressively for 48 h following LH stimulation and remained elevated in fully luteinized cells at 96 h. This increase in PRL receptor appears to be functionally related to the ability of luteal cells to respond to PRL. When PRL was given for 4 days after LH, both luteal cell progesterone production and LH receptor content increased progressively after, but not before, 48 h. Since these changes occurred in the absence of LH, the increase in LH receptor appears to be a consequence of, but not a requirement for, the PRL-induced increase in progesterone production. If daily injections of PRL were delayed for 72 or 96 h following LH induction of lutenization, luteolytic rather than luteotropic effects of PRL were observed. Since receptor for PRL remained elevated at 72 and 96 h, intracellular mechanisms and not receptor content, appear to be effecting the response of luteal cell to PRL.

20-alpha-Dihydroprogesterone↗
PubMed1998

Absence of increased neuropeptide Y neuronal activity before and during the luteinizing hormone (LH) surge may underlie the attenuated preovulatory LH surge in middle-aged rats.

A large body of evidence suggests that the neuroendocrine axis plays a major role in the reproductive aging of female rats. Since increased hypothalamic neuropeptide Y (NPY) neurosecretion is crucial in the preovulatory LH discharge in young rats, we tested the hypothesis that diminution in the preovulatory LH surge in middle-aged (MA) rats may be due to altered neurosecretory activity in NPYergic neurons. In Exp 1, we examined NPY levels in six microdissected hypothalamic nuclei, including median eminence (ME), arcuate nucleus (ARC), and medial preoptic area (MPOA), at 1000, 1200, 1400, 1600, 1800, 2000, or 2200 h on the day of proestrus in young (2.5- to 3-month old) and MA (7- to 9-month old) regularly cycling rats. At 1000 h, ME NPY levels in young rats were significantly lower than those in MA rats. In young rats, the ME NPY levels were significantly increased at 1400 h before the LH surge in the afternoon and thereafter decreased progressively during the interval of the LH surge. In MA rats, however, ME NPY levels decreased in the afternoon in association with an attenuated LH surge. In addition, in the ARC and MPOA, the other hypothalamic sites associated with induction of LH surge, NPY levels increased before and during the LH surge in young rats, no change in NPY levels in these nuclei was observed in association with the attenuated LH surge in MA rats. Also, NPY levels in the ARC and MPOA during the afternoon were significantly lower in MA compared with those in young animals. These results demonstrated the absence of an antecedent increase in NPY levels, specifically in the ME and ARC, during the afternoon of proestrus in MA animals. In a second experiment, we evaluated whether the absence of dynamic changes in NPY levels in the ME and ARC in MA rats was due to altered hypothalamic NPY gene expression. Regularly cycling young (2.5- to 3-month-old) and MA (8- to 10-month-old) rats were killed at 1000, 1200, 1400, 1600, 1800, 2000, or 2200 h on the day of proestrus. The medial basal hypothalamus was processed for prepro-NPY messenger RNA (mRNA) measurement by ribonuclease protection assay. In young rats, prepro-NPY mRNA levels were significantly increased at 1200 h and remained elevated throughout the afternoon. In contrast, in MA rats prepro-NPY mRNA levels remained unchanged before and during the attenuated LH surge. These results clearly indicate that the augmentation in NPY neuronal activity before and during the LH surge seen in young rats fails to manifest itself in middle-aged rats. As hypothalamic NPY participates in the induction of LHRH surge, our results suggest that reduced LHRH and LH surges in MA rats may be due to diminution in NPY secretion in these animals.

Aging↗
PubMed2000

Luteinizing hormone (LH) drives diverse intracellular calcium second messenger signals in isolated porcine ovarian thecal cells: preferential recruitment of intracellular Ca2+ oscillatory cells by higher concentrations of LH.

The present study examines Ca2+ second messenger signaling driven by LH in isolated porcine thecal cells. To this end, we implemented semiquantitative fluorescent (fura-2) videomicroscopic imaging of single thecal cells in vitro. Stimulation of 388 cells with LH (5 microg/ml) elicited an intracellular Ca2+ ([Ca2+]i) signal in 85+/-5.3% of individual thecal cells (n = 11 experiments). Among 337 LH-responsive cells, we identified four predominant temporal modes of [Ca2+]i signaling: 1) [Ca2+]i oscillations with periodicities of 0.5 to 4.5 min(-1) (63+/-4.5%), 2) a [Ca2+]i spike followed by a sustained plateau (17+/-2.6%), 3) a [Ca2+]i spike only (5.8+/-2.6%); and 4) a [Ca2+]i plateau only (3.8+/-1.5%). The prevalence, but not the amplitude or frequency, of LH-induced [Ca2+]i oscillations in thecal cells was dependent on the agonist concentration. Reduced availability of extracellular Ca2+ induced by treatment with EGTA or cobaltous chloride did not block the initiation, but reversibly abolished ongoing [Ca2+]i oscillations (72% of cells) or increased the mean [Ca2+]i interspike periodicity from 1.09+/-0.16 to 0.59+/-0.07 min(-1) (P < 0.05). Putative phospholipase C inhibition with U-73122 (10 microM) also abolished or frequency-damped LH-driven [Ca2+]i oscillations in 95+/-4.7% of cells. [Ca2+]i oscillations in thecal cells were not abrogated by overnight pretreatment with pertussis toxin. We conclude that 1) thecal cells (unlike earlier findings in granulosa cells) manifest a diverse array of [Ca2+]i signaling responses to LH at the single cell level; 2) LH can dose dependently recruit an increasing number of individually [Ca2+]i oscillating thecal cells; 3) extracellular Ca2+ is required for LH to sustain (but not initiate) frequent and high amplitude [Ca2+] oscillations in thecal cells; and 4) these signaling actions of LH are mediated via phospholipase C, but not a pertussis-toxin sensitive mechanism. Accordingly, the present data extend the apparent complexity of LH-induced [Ca2+]i second messenger signaling and identify at the single cell level LH's dose-responsive drive of [Ca2+]i oscillations in gonadal cells.

Animals↗
PubMed1991

Luteinizing hormone (LH) secretory burst duration is independent from LH, prolactin, or gonadal steroid plasma levels in amenorrheic women.

The possible presence of LH pulsatile secretion has been studied in patients with hypothalamic amenorrhea [LH plasma levels, less than 3 (n = 35) or greater than 3 IU/L (n = 18)], amenorrhea associated with hyperandrogenemia (n = 31), or hyperprolactinemia (n = 10). Patients were sampled every 10 min for 4 h, and LH plasma concentrations were determined by the use of an immunofluorimetric assay. The program Detect was used for both pulse detection and data deconvolution, i.e. for instantaneous secretory rate computation, on LH time series. The presence of episodic LH secretion was observed in all patients, and LH pulse frequency ranged between 3.5 +/- 0.3 and 3.8 +/- 0.2 peaks/4 h among the four groups. LH pulse amplitude was significantly reduced in patients affected by hypothalamic amenorrhea with LH plasma levels lower than 3 IU/L (0.7 +/- 0.1 IU/L; P less than 0.01) and significantly increased in patients with hyperandrogenic amenorrhea (6.8 +/- 0.3 IU/L; P less than 0.01) compared to levels in the other groups under study. Instantaneous secretory rate computation permitted the optimal resolution of the secretory events and demonstrated that the duration of gonadotrope secretory bursts ranged from 22.8 +/- 1.4 to 26.8 +/- 2.3 min in amenorrheic patients and did not depend on LH, PRL, or sex steroid plasma levels. In conclusion, the present study shows the presence of significant LH pulsatile release in amenorrheic patients, suggesting that in amenorrheic, as in normally cycling, women the secretory bursts from the gonadotropes have the same duration, despite the plasma LH, PRL, or steroid hormone levels.

Adolescent↗
PubMed1992

Concordant suppression of serum immunoreactive luteinizing hormone (LH), follicle-stimulating hormone, alpha subunit, bioactive LH, and testosterone in postmenopausal women by a potent gonadotropin releasing hormone antagonist (detirelix).

The purposes of the current study were 2-fold: 1) to assess the effects of a new antagonistic analog of GnRH [N-Ac-D-Nal(2)1, D-pC1-phe2, D-Trp3, D-hArg (Et2)6, D-Ala10] GnRH, or detirelix (Syntex Research) on gonadotrope function as reflected by serum levels of immuno- and bioassayable LH, and immunoactive FSH and alpha-subunit concentrations in postmenopausal, hypergonadotropic women; and 2) to determine if androgen production in the postmenopausal ovary is gonadotropin dependent. Six normal postmenopausal women were studied. Each volunteer received doses of 1, 5, and 20 mg detirelix sc in a random order separated by at least a 1-week interval. Serum LH, FSH, and alpha-subunit were measured by RIA at frequent intervals for 72 h after each injection. Bioactive LH levels were measured at 0, 24, 48, and 72 h after injection by a mouse Leydig cell bioassay, to permit comparison of biological with immunological LH activity. The steroids testosterone (T) and dehydroepiandrosterone sulfate were measured before injection and 12 (T only), 24 and 48 h after injection of the 20 mg dose. Immunoactive levels of serum LH and FSH were both suppressed in a dose-dependent manner, but LH suppression was greater than that of FSH. Maximum LH suppression (mean +/- SEM) after the 1, 5, and 20 mg doses was 40.2 +/- 7.0%, 63.2 +/- 3.4%, and 75.8 +/- 2.2%, respectively. For the same doses, maximum FSH suppression was 18.0 +/- 6.0%, 25.6 +/- 4.6%, and 39.6 +/- 2.7%. LH levels remained suppressed below baseline for up to 72 h after the 20 mg dose. Bioactive LH changes closely paralleled those of immunoactive LH. Mean LH suppression (area under the serum concentration curve) during the first 24 h after injection was 23.5 +/- 6.2% for the 1-mg dose, 47.2 +/- 4.7% for the 5-mg dose, and 61.0 +/- 2.1% for the 20-mg dose. Mean percent FSH suppression during the first 24 h, calculated in the same manner, was 6.8 +/- 3.9% (1 mg), 14.5 +/- 2.9% (5 mg), and 18.2 +/- 2.6% (20 mg). Serum alpha-subunit concentrations were significantly suppressed by 1 h after dosing with the 5- and 20-mg doses (P less than 0.05), and remained suppressed throughout the 72-h sampling period. Gonadotropin dependence of steroidogenesis in the postmenopausal ovary was suggested by a significant suppression of serum T concentrations after the 20-mg dose of detirelix.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1994

Identification of two point mutations in the gene coding luteinizing hormone (LH) beta-subunit, associated with immunologically anomalous LH variants.

To analyze the structure of LH in three patients with immunologically anomalous LH, the whole coding region of the LH beta-subunit gene was examined. These patients were infertile, and their serum LH levels could not be measured with an immunoassay kit. Immunoblotting of the LH beta-subunit showed no marked changes in the molecular size of LH beta. Genomic DNA was extracted from peripheral lymphocytes of the patients and normal controls, and LH beta genes were amplified by the polymerase chain reaction technique, using primer pairs that are capable of specifically amplifying only the LH beta gene without interference by the CG beta genes. No deletions were observed in the coding regions of the LH beta gene of the patients. Nucleotide sequencing revealed two nucleotide substitutions in the LH beta gene of the patients, which cause amino acid replacements from Trp8 (TGG) to Arg8 (CGG) and Ile15 (ATC) to Thr15 (ACC). Restriction fragment length polymorphism analysis in three families indicated that the affected probands were homozygous, and their family members were heterozygous, except for their husbands. The heterozygotes showed reduced detectability with the LH immunoassay kit. These results suggest that these amino acid replacements are responsible for this immunologically anomalous variant.

Adult↗
PubMed1979

LH and testosterone release in developing bulls following LH-RH treatment. Effect of gonadectomy and chronic testosterone propionate pre-treatment.

LH and testosterone release after LH-RH treatment was studied in male calves from 1 week to 8 months of age. Total LH release, LH peak values and duration of the discharge increased from 1 week to 4 months of age by 406, 453 and 110%, respectively. Significant decreases of 54, 48 and 24% were observed at 6 months of age compared to 4 months of age. This was followed by steep increases in those variables of 344, 129 and 69% at 8 months compared to 4 months. A testosterone response following an LH increase was first seen at 4 months of age when a weak discharge occurred in 2 out of 5 calves. In older calves strong and LH-correlated testosterone responses were always observed. In a second experiment the LH response to LH-RH was studied in 6 months old calves castrated 2 months previously. The total LH response was 61% greater than in intact controls. When animals were castrated and pre-treated briefly with testosterone propionate the response was increased by 183% and the time to reach the LH peak was increased by 360%. From these and other results a synthesis of endocrine events during the first year of life is proposed. In particular it seems that the period between 4 and 8 months of age is crucial since interactions between steroid feedback and pituitary sensitivity to LH-RH change and eventually reach an equilibrium.

Age Factors↗
PubMed1981

Effect of oestrogen and an LH-RH agonist on the release of gonadotrophins in ovariectomized ewes deprived of LH-RH.

Endogenous LH-RH in ewes was inhibited by active immunization or by injection of LH-RH antiserum. Plasma levels of LH and FSH were elevated in 3 ovariectomized control ewes but low in 3 LH-RH immunized ovariectomized ewes. Oestradiol benzoate (50 microgram i.m.) caused a marked rise in LH concentrations in control ewes but not in the immunized ewes. In the immunized ewes the low plasma levels of FSH decreased even further 8-36 h after injection of oestrogen, indicating a direct inhibitory action of the steroid on the pituitary. Both groups responded to the oestrogen injection by a rise in plasma levels of prolactin and by exhibiting normal oestrous behaviour. When the control ewes were again challenged with oestradiol benzoate and, after 10 h, given an i.v. injection of 75 ml antiserum to LH-RH, the LH surge was abolished in one animal and reduced in another. These experiments indicate that the continued presence of LH-RH is necessary for the occurrence of the oestrogen-induced LH surge in the ewe. Administration of a stimulatory analogue of LH-RH released LH and FSH in control and immunized ewes but the responsiveness to further injections at intervals of 3 h decreased, particularly for FSH.

Animals↗
PubMed1988

Continuous infusion of GnRH reduces the LH response to an intravenous GnRH injection but does not inhibit endogenous LH secretion in cows.

Plasma LH concentrations were monitored in 6 Hereford X Friesian suckled cows at about 80 days post partum, before and during a 14-day period of continuous s.c. infusion of GnRH (20 micrograms/h). Blood samples were collected at 10-min intervals on Days -2, -1, 1, 2, 3, 4, 7, 10, 13 and 14 (Day 1 = start of infusion). Plasma LH concentrations rose from mean pretreatment levels of 1.3 +/- 0.20 ng/ml to a maximum of 17.1 +/- 3.09 ng/ml within the first 8 h of GnRH infusion, but returned to pretreatment levels by Day 2 or 3. In 4/6 animals, the initial increase was of a magnitude characteristic of the preovulatory LH surge. In all animals, an i.v. injection of 10 micrograms GnRH, given before the start and again on the 14th day of continuous infusion, induced an increase in LH concentrations but the increase to the second injection was significantly (P less than 0.01) less (mean max. conc. 6.4 +/- 0.76 and 2.3 +/- 0.19 ng/ml). Mean LH concentrations (1.0 +/- 0.08, 1.1 +/- 0.08 and 0.9 +/- 0.06 ng/ml) and LH episode frequencies (3.3,4.3 and 3.2 episodes/6 h) did not differ significantly on Days -2,7 and 13. However, the mean amplitude of LH episodes was significantly lower (P less than 0.05) on Day 13 (1.3 +/- 0.10 ng/ml) than on Day -2 (1.8 +/- 0.16 ng/ml). Therefore, although the elevation in plasma LH concentrations that occurs in response to continuous administration of GnRH is short-lived and LH levels return to pre-infusion values within 48 h of the start of infusion, these results show that the pituitary is still capable of responding to exogenous GnRH, although the LH response to an i.v. bolus injection of GnRH is reduced. In addition, this change in pituitary sensitivity is not fully reflected in endogenous patterns of episodic LH secretion.

Animals↗
PubMed1997

Effect of oestradiol replacement in ovariectomized chickens on pituitary LH concentrations and concentrations of mRNAs encoding LH beta and alpha subunits.

Plasma concentrations of oestradiol and LH and steady-state pituitary concentrations of the mRNAs encoding the LH beta and alpha subunits in the gland were measured at intervals of 1 month for 5 months in female chickens. In addition, feedback regulation by oestradiol of concentrations of mRNAs encoding these LH subunits was studied in ovariectomized young (3-week-old) and adult hens. Concentrations of the mRNAs encoding the LH beta and alpha subunits increased significantly before sexual maturity and the changes were highly correlated with increases in plasma and pituitary concentrations of LH. Ovariectomy significantly reduced circulating plasma concentrations of oestradiol but increased pituitary concentrations of mRNAs encoding LH beta and alpha subunits and pituitary and plasma concentrations of LH in adult laying hens. In addition, in 3-week-old chickens, ovariectomy induced an increase in plasma and pituitary gland concentrations of LH. This ovariectomy-induced mRNA expression and tissue and plasma increases of LH were prevented by oestradiol replacement. These data suggest that a negative feedback mechanism by ovarian oestradiol inhibits LH release from the pituitary and pituitary LH biosynthesis in chickens.

Animals↗
PubMed1984

Decreased in vitro LH releasing activity of oligomeric LH-RH derivatives.

Primary rat pituitary cell culture system was used to investigate LH releasing activity of dimeric and oligomeric LH-RH agonists. In addition, peptides containing both agonistic as well as inhibitory segments were tested in order to find out which sequence overrules the other part of the molecule. In addition, intracellular cAMP levels were determined. All peptides but D-Phe2, D-Trp3, D-Lys6-LH-RH which was noted to be an inhibitor were found to increase intracellular cAMP contents. Only 72% LH releasing activity of LH-RH was registered for the analog which was composed of an agonistic and inhibitory chain. Dimeric and tetrameric derivatives of D-Lys6-LH-RH exhibited significantly lower LH releasing activity than the parent compound. But, no differences between the dimer and tetramer with agonistic chains was noted. The data show that cAMP may be involved in certain steps of LH-RH induced LH release, but does not play a role in overall LH release. In addition, dimerization and tetramerization of LH-RH agonist chains by short bridges is not sufficient for binding to more than one receptor molecule. Such derivatives could, however, reveal the length of the connecting bridge which is necessary for inducing receptor aggregation.

Animals↗
PubMed2000

Effect of estradiol and progesterone on oviductal LH-receptors and LH-dependent relaxation of the porcine oviduct.

We have previously shown that the porcine oviduct possesses immunoreactive and functional LH receptors and that LH causes relaxation of the oviduct, especially during the periovulatory stage of estrous cycle. The current studies were undertaken to investigate the effects of estradiol and progesterone on LH receptor protein and LH-stimulated motility of the oviduct in steroid-primed ovariectomized gilts. Twenty-one cross-bred gilts were ovariectomized at 6 m.o. of age. Four weeks later gilts received daily intramuscular injection of either 2 mL corn oil (control n = 4), estradiol benzoate (EB) 1.5 mg (n = 6), progesterone 50 mg (n = 5), or 1.5 mg EB plus 50 mg progesterone (n = 6) for 4 consecutive days. The gilts were slaughtered on Day 5 after the first injection of steroids or vehicle. Rings of isthmus and ampulla were collected from each oviduct and placed in a tissue chamber perfused with Kreb's solution for 60 min. The mechanical activity was recorded for 30 min after LH treatment. Immunoreactivity of LHR in the Fallopian tube sections were detected in the epithelium of the tubal mucosa, smooth muscle cells and the blood vessel endothelium. Western blotting showed that porcine oviducts contain 75, 48 and 45 kDa immunoreactive LH receptor proteins, like the corpus luteum (CL). The lowest receptor expression was found in controls and in gilts treated with estradiol or progesterone. Combined treatment with estradiol and progesterone resulted in a significant increase of LH receptor protein concentrations when compared with control animals. In vitro LH treatment affected oviduct contractility of combined estradiol and progesterone treated gilts but not the oviduct of the remaining groups. It also caused a decrease in amplitude, frequency and areas under the curve (AUC) of ampulla (P < 0.05) and the amplitude and AUC of isthmus (P < 0.001) in combined estradiol and progesterone-primed gilts. These results indicate that estradiol and progesterone together, but not separately, increase LH receptor protein in the porcine oviduct and that combined estradiol and progesterone priming is necessary for LH-induced relaxation of the porcine oviduct.

Animals↗