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PubMed1984

Prostaglandin F2 alpha inhibits luteinizing hormone (LH)-induced increase in LH receptor binding to isolated rat luteal cells.

The effect of the luteolytic hormone prostaglandin F2 alpha (PGF2 alpha) on parameters of LH receptor binding to isolated rat luteal cells was examined. The equilibrium binding constant (0.55 X 10(10) M-1), the association rate constant (0.89 X 10(8) M min-1), and the dissociation rate constant (1.70 X 10(-2) M min-1) were not significantly altered by PGF2 alpha. However, as [125I]iodohCG binding approached equilibrium (less than 2 h) and at equilibrium (greater than 3 h), PGF2 alpha, but not PGE2, consistently reduced LH binding by 10-20%. The LH receptor-binding capacity, determined by Scatchard analysis of [125I]iodo-hCG or [125I]iodo-hLH binding, was reduced from 7.5 +/- 0.1 to 6.4 +/- 0.1 X 10(4) receptors/cell in the presence of PGF2 alpha. This reduction of total cell-bound radioactivity by PGF2 alpha was not due to a change in the rate of hormone internalization and degradation. However, when cells were briefly treated with a pulse of LH (5 ng/ml; 5-10 min), [125I] iodo-hCG (LH) binding increased 20-30% within 2 h, and PGF2 alpha prevented this LH-induced increase. A similar pulse of cAMP analogs did not alter LH binding. We conclude that while the initial binding of LH to its receptor is not altered by PGF2 alpha, it does reduce the final equilibrium level of LH binding by a mechanism that involves a block in the appearance of LH-induced cryptic receptors.

Animals↗

PubMed1995

Effects of luteinizing hormone (LH) and androgen on steady state levels of messenger ribonucleic acid for LH receptors, androgen receptors, and steroidogenic enzymes in rat Leydig cell progenitors in vivo.

Adult Leydig cells differentiate postnatally from mesenchymal-like progenitor cells. The relative scarcity of LH receptors (LHRs) in progenitor cells indicates that additional hormones may be important in the initial phases of Leydig cell differentiation. High levels of androgen receptor (AR) in progenitor cells point to a role for androgen in these cells. In the present study, an LHRH antagonist, [Ac-D2Nal1,4C1DPhe2,D3Pal3,Arg5,DGlu6(anis ole adduct), DAla10]GnRH (NalGlu; 250 micrograms/kg body weight), was used to suppress endogenous secretion of both LH and androgen during days 14 to 21 postpartum in vivo. To examine the effects of LH and androgen on regulation of Leydig cell progenitors (PLCs), exogenous LH (5 micrograms/day), testosterone (T; 30 micrograms/day), or both were administered to NalGlu-treated rats. After 7 days of treatment, we examined the effects on testis weight, Leydig cell morphology, and T production. The steady state messenger RNA (mRNA) levels for LHR, AR, cytochrome P450 17 alpha-hydroxylase, and 3 alpha-hydroxysteroid dehydrogenase in purified PLCs were measured by reverse transcription-polymerase chain reaction, with ribosomal protein S16 as the internal control. Treatment with NalGlu significantly decreased testis weight, resulted in an abundance of mesenchymal-like cells over immature Leydig cells, lowered T production, and reduced the levels of several Leydig cell mRNAs. Treatment with exogenous LH or T maintained testis weight and Leydig cell morphology in NalGlu-treated rats. The mRNA levels for LHR, AR, and 3 alpha-hydroxysteroid dehydrogenase were significantly increased by LH or T. P450 17 alpha-hydroxylase mRNA levels were elevated by LH to control level but strikingly reduced by T. Combined treatment with LH and T further increased basal T production but did not elevate mRNAs beyond the levels obtained with each hormone alone. LH and androgen act similarly in PLCs in promoting Leydig cell differentiation with respect to morphological and molecular landmarks. These findings support the hypothesis that androgen as well as LH is involved in the differentiation of immature Leydig cells from mesenchymal-like progenitors.

3-Hydroxysteroid Dehydrogenases↗

PubMed2001

Adenovirus-directed expression of functional luteinizing hormone (LH) receptors in undifferentiated rat granulosa cells: evidence for differential signaling through follicle-stimulating hormone and LH receptors.

This study was conducted to determine the feasibility of using replication-defective adenovirus vectors to express receptors for LH. Two vectors were constructed, one that directs the expression of wild-type human LH receptor (LHr; AdRSVLHrwt) and another that directs the expression of the constitutively activated D578H mutant human LH receptor (AdRSVD578HLHr). When infected with AdRSVwtLHr and AdRSVD578HLHr, COS-1 cells expressed LH/hCG-binding sites as reflected by specific binding of [(125)I]hCG. To determine the ability of the vectors to confer LH responsiveness, undifferentiated rat granulosa cells, which possess only FSH receptors, were infected with AdRSVwtLHr and AdRSVD578HLHR: Expression of the constitutively activated D578H LHr increased basal (gonadotropin-independent) estrogen and progesterone production. Expression of the wild-type LHr in granulosa cells did not stimulate basal steroid production, but conferred responsiveness to exogenous LH. For both wild-type LHr and D578HLHr, the absolute levels of steroid production were dependent upon the input of viral titers. Using these vectors, we compared effects of FSH and LH receptor activation in undifferentiated granulosa cells. Stimulation of undifferentiated granulosa cells by FSH and D578HLHr, as well as activation of wild-type LHr with LH resulted in comparable production of progesterone. In contrast, estradiol production in cells stimulated with FSH was greater than that in cells that expressed either D578H receptors or wild-type LHr in the presence of LH. Analysis of messenger RNAs (mRNAs) revealed that activations of FSH and the LH receptors were comparable in the induction of alpha-inhibin and 3betahydroxysteroid dehydrogenase mRNAS: However, activation of FSH receptor led to significantly greater expression of P450 aromatase and LHr mRNAs than did activation of LHR: These results suggest that activation of FSH and LH receptors in granulosa cells may differ with respect to activating intracellular signaling pathways and stimulating gene expression.

8-Bromo Cyclic Adenosine Monophosphate↗

PubMed1991

Binding sites for LH in Candida albicans: comparison with the mammalian corpus luteum LH receptor.

We have described recently the presence of binding sites for human LH (hLH) and human chorionic gonadotrophin (hCG) in microsomal and cytosol fractions prepared from the dimorphic, pathogenic fungus, Candida albicans. We have now compared the properties of Candida LH/hCG-binding sites with those of the ovine luteal LH receptor. Sheep luteal LH-binding sites were associated with luteal membranes, and little or no binding activity was present in cytosol fractions. In contrast, significant LH/hCG-binding activity was present in Candida cytosol. Moreover, there were marked differences in sensitivity to inhibition by metal ions, association and dissociation rates, and affinity constants between sheep and Candida LH-binding sites. Scatchard plots of 125I-labelled hLH binding to sheep luteal receptors demonstrated a single high-affinity component (association constant (Ka) 0.3 litres/pmol) which was displaceable by hCG. In contrast, Scatchard plots of binding to Candida microsomes and cytosol fractions demonstrated two components, one with high affinity (Ka 0.18 litres/pmol) and low capacity and a second site with lower affinity (Ka 4 litres/nmol) and high capacity, both of which were displaceable by unlabelled hCG. Gel permeation chromatography of cytosol demonstrated two distinct peaks of LH-binding activity with approximate molecular weights of greater than 1,000,000 and 30,000-50,000. Scatchard plots of 125I-labelled hLH binding to the higher molecular weight peak demonstrated a single, high-affinity LH-binding site (Ka 0.18 litres/pmol), whereas the lower molecular weight fraction contained both high- (Ka 0.17 litres/pmol) and low-affinity (Ka 4 litres/nmol) LH-binding sites. Both partially purified and highly purified hCG and hLH preparations displaced binding of 125I-labelled hLH and hCG to sheep luteal LH receptors at similar concentrations. 125I-labelled hLH/hCG binding to Candida membranes was also displaceable by low levels (ng) of partially purified hCG preparations, but much higher levels (micrograms) of highly purified hLH and hCG were required. This paradoxical observation suggested the presence of radiolabelled contaminants, or damaged forms induced during radioiodination of hormone tracers, which can bind more strongly to Candida membranes than unlabelled hCG and hLH but which do not bind to sheep LH receptors. However, no evidence for hLH tracer contaminants with differential binding to Candida and sheep luteal receptors was obtained following gel exclusion chromatography or fractionation on Concanavalin A-Sepharose. (Although three distinct 125I-labelled hLH fractions were resolved on Concanavalin A-Sepharose, presumably reflecting differences in their carbohydrate compositions, all three tracer peaks bound equivalently to both Candida membranes and ovine luteal LH receptors).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1984

Time- and dose-dependent alterations of basal and LH-RH-stimulated LH-release during treatment with various hormonal contraceptives.

The dose- and time-dependent effect of treatment with estrogen and progestogens on serum LH before and 15 min. after the i.v. injection of 150 ng LH-RH was investigated in intact female rats. The animals were injected s.c. daily with ethinyl estradiol (EE), levonorgestrel (NG), desogestrel (DG), norethisterone (NET), chlormadinone acetate (CMA) or cyproterone acetate (CPA) alone or in various combinations, and LH was measured after 1, 2, 3, and 4 weeks of treatment and 2 weeks after termination of the injections. The treatment with low- and high-dosed combined preparations caused a marked decrease of basal LH levels which was not reversed 2 weeks after discontinuation. The combination of 30 and 50 micrograms EE with 125 or 250 micrograms NG was more effective in depressing LH-RH-induced LH release than that with 125 or 250 micrograms DG which were, however, reversible in all cases. The increase in the estrogen dose intensified the suppressive effect to a greater extent than the doubling of the progestogen dose. The suppression of the LH-RH-stimulated LH release occurred in a time-dependent manner; there was, however, a transitory amplification after 1 week when 50 micrograms EE/125 micrograms DG were tested. The high-dosed combinations of 50 micrograms EE with 500 micrograms NG, 2 mg NET, 2 mg CMA or 2 mg CPA brought about a very strong blockade of both basal and LH-RH-induced LH secretion which persisted 2 weeks after termination of treatment. The results indicate that even minor alterations in the doses of the estrogen and progestogen components of combined oral contraceptives (OC) may lead to considerable differences in the functional stage of the gonadotrophs which also depend on the duration of treatment.

Animals↗

PubMed1984

A comparison of the LH-releasing activities of LH-RH and its agonistic analogue buserelin in the ovariectomized rat.

LH-RH and the potent agonistic analogue (D-Ser(But)6-des-Gly10)-LH-RH(1-9)-ethylamide (HOE-766 or buserelin) were at several doses either infused or injected intravenously in 5-weeks-ovariectomized rats, which had been treated with either 3 micrograms estradiol-benzoate (EB) or with oil, 24 h previously. Blood samples for assay of LH were taken during the subsequent 24 h. Pituitary glands were removed at the end of the experiments. Buserelin, when infused, was slightly more effective than LH-RH on releasing LH. When injected, however, buserelin was at the higher dose ranges increasingly more effective as an LH-releasing agent than LH-RH. EB-treatment increased the LH response of the pituitary gland to both peptides in an identical way. It was concluded that buserelin derives its high potency not from its intrinsic LH-releasing activity, which is only slightly greater than that of LH-RH, but from a longer duration of action.

Animals↗

PubMed1977

Steroid and FSH action on LH receptors and LH-sensitive testicular responsiveness during sexual maturation of the rat.

This study examines the effect of FSH, testosterone and estradiol on testicular LH receptors and in vitro testicular responsiveness to LH in immature rats under various conditions. FSH treatment of 15-day-old immature rats significantly increased the number of LH receptors but did not alter testicular responsiveness. FSH treatment of hypophysectomized immature rats increased the number of LH receptors and markedly increased testicular responsiveness. Treatment of hypophysectomized rats with testosterone proprionate for 4 days, followed by a 5-day treatment with FSH, enhanced the effect of FSH on the number of LH receptors but did not increase the effect of FSH on testicular responsiveness. In contrast, treatment with estradiol for 4 days before FSH treatment had no effect on the FSH-induced increase in LH receptors but completely inhibited the FSH-induced increase in testicular responsiveness. These observations suggest that during male sexual maturation (1) regulation of LH receptors is distinct from regulation of testicular responsiveness to LH, (2) estradiol may be a factor in the regulation of testicular responsiveness to LH, and (3) testosterone may enhance the FSH-induced increase of LH receptors.

Animals↗

PubMed1976

Correlation between leuteinizing hormone responses to luteinizing hormone-releasing hormone (LH-RH) and to D-leu-6-LH-RH-ethylamide in patients with hypothalamo-pituitary disease.

Seventeen patients (eleven females and six males) with organic hypothalamo-pituitary disease were subjected to a test consisting of a rapid intravenous injection of 50 mug of luteinizing hormone-releasing hormone (LH-RH) at 8:00 A.M., with blood sampling before and 30 and 60 minutes afterward. Two to four weeks later, a rapid intravenous injection of 50 mug of D-Leu-6-des-Gly-10-LH-RH-ethylamide (D-Leu-6-LH-RH-EA) was given under similar conditions, with blood sampling before and 30, 60, and 90 minutes afterward. Serum LH levels were determined by radioimmunoassay. D-Leu-6-LH-RH-EA caused a greater and more sustained rise in serum LH levels than did an equal dose of LH-RH. However, functional classifications of patients were similar with either preparation. This finding suggests that acute administration of D-Leu-6-LH-RH-EA does not cause a higher number of relevant responses as compared with LH-RH, but only a greater stimulation of LH releases in responsive patients.

Adenoma, Acidophil↗

PubMed1977

Luteinizing hormone (LH), follicle-stimulating hormone, and testosterone responses to consecutive injections of D-leucine-6-LH-releasing hormone ethylamide in normal men.

Luteinizing hormone (LH), follicle-stimulating hormone (FSH), and testosterone (T) responses to three consecutive intravenous injections of D-Leu-6-LH-releasing hormone ethylamide (D-Leu-6-LH-RH-EA) at 3-hour intervals were studied in six healthy, fertile, male volunteers 34.2+/-1.6 years of age. Each man received three injections of 20 microng of D-Leu-6-LH-RH-EA at 6:00 A.M., 9:00 A.M., and 12:00 noon, respectively. Blood samples were obtained before the first injection and at 1, 2, 3 (before the second injection), 4, 5, 6 (before the third injection), 7, 8 and 9 hours after the beginning of the test. Serum levels of LH, FSH, and T were determined by radioimmunoassay with the double-antibody technique. The response to the first injection of D-Leu-6-LH-RH-EA confirmed the longer duration of the stimulation of LH and FSH release caused by this compound as compared with that caused by LH-RH. Serum T levels rose significantly, almost paralleling the variations experienced with gonadotropins. The second injection caused a slight increase in LH and T responses in relation to the first injection. Two and three hours after administration, the third stimulus resulted in hormone levels lower than those obtained with the first two injections. Possible explanations for this finding might be a reduction of pituitary responsiveness as a result of multiple stimulation with D-Leu-6-LH-RH-EA, or spontaneous circadian variation of the pituitary response, or a combination of factors.

Adult↗

PubMed1997

Use of a GnRH antagonist in conjunction with low amplitude, high frequency LH pulses to induce follicular growth without an LH surge and ovulation in ewes.

The present study was undertaken to develop an experimental sheep model which could be used to investigate the abnormal follicle growth that is associated with the absence of the LH surge. On Day 10 of the oestrous cycle, 16 ewes were treated with an analogue of prostaglandin (cloprostenol; PG) and blood sampled every 4 h thereafter to determine the normal timing of the preovulatory LH surge. Three oestrous cycles later, all ewes were simultaneously treated with PG and a gonadotrophin-releasing hormone (GnRH) antagonist ([Ac-DNal1, D4C1Phe2, DTrp3, DArg6, DAla10] GnRH.HOAc; 50 micrograms kg-1 subcutaneously). Group 1 ewes (n = 6) received no further treatment. Group 2 ewes (n = 5) were additionally treated for a total of 7 days, starting at the time of PG injection, with purified ovine luteinising hormone (LH; preparation P 3 R3-5; equivalent to 1.25 micrograms NIH-oLH-S26) administered i.v. over a 2 min period. For the first 24 h, LH was given at 3 h intervals for 12 h, then every 2 h for 12 h, and thereafter hourly for 6 days. Group 3 ewes (n = 5) were treated as Group 2 but at 72 h received an additional antagonist injection (50 micrograms kg-1 subcutaneously). Mean values of LH from 24 to 96 h were significantly lower in untreated controls and Group 1 than in the other two groups (0.58 +/- 0.2 ng ml-1 and 0.55 +/- 0.2 ng ml-1 vs. 1.63 +/- 0.5 and 1.68 +/- 0.6 ng ml-1, respectively; P < 0.01). After treatment with PG alone in the untreated control group, the preovulatory LH surge began in all ewes at 59.9 +/- 2.8 h after PG. All Group 1 ewes also had an LH surge but the period from PG injection to the onset of the surge was 124 +/- 17.3 h (range 96-152 h). Only two of the Group 2 ewes had an LH surge (at 160 and 168 h, respectively) and no surge was detected in Group 3 ewes. In Group 1, mean values of follicle-stimulating hormone (FSH; 0.78 +/- 0.07 ng ml-1) were not affected by treatment with antagonist alone; however, in the two groups receiving exogenous LH pulses there was a marked decrease in FSH concentrations during the period 24-96 h. Progesterone concentrations increased 9 days after PG treatment in five out of six ewes in Group 1. In Group 2, there was evidence of a variable luteinisation response, but in Group 3 progesterone remained less than 0.08 ng ml-1 throughout. Endoscopy 112-115 h after PG confirmed that none of the 16 antagonist-treated ewes had ovulated; an event normally expected approximately 80 h after PG in sheep. The experimental protocol of Group 3 provides the basis for a model which will enable examination of the long-term functional capacity of ovarian follicles which have not been exposed to an LH surge.

Analysis of Variance↗

PubMed1995

Characteristics of urinary luteinizing hormone (LH) during the induction of LH surges of different magnitude in blood.

Urinary luteinizing hormone (LH) testing has been proposed as a reliable method for the prediction of ovulation but its accuracy has been challenged by some studies. To check how accurately the oscillations of urinary LH reflected the plasma changes, surges of LH of different magnitude and duration were artificially induced in plasma and the hormone was measured simultaneously in urine. Post-menopausal women (n = 16) were stimulated during 1 week with a combination of transdermal oestradiol (400 micrograms) and i.m. progesterone (25 mg on day 4, 50 mg on day 5) to obtain an LH discharge comparable with the pre-ovulatory LH peak. A short and moderate peak of LH was induced by the i.v. injection of 100 micrograms gonadotrophin-releasing hormone (GnRH) in six premenopausal women, whereas an LH discharge of higher amplitude and longer duration was induced by a single dose of 0.3 mg s.c. buserelin. The total urine production of the day was fractionated into 8 h periods. LH was measured by a commercial radioimmunoassay. Unambiguous peaks of LH were detected in the urine of all the women stimulated with either oestradiol plus progesterone or buserelin, but in only three out of the six women receiving GnRH. The urine LH reproduced the plasma changes of the hormone with short delay since the peaks were mostly detected in the same time fraction in which the serum discharge occurred.

Adult↗

PubMed1985

Seasonal changes in pulsatile luteinizing hormone (LH) secretion in the ewe: relationship of frequency of LH pulses to day length and response to estradiol negative feedback.

Seasonal changes in pulsatile luteinizing hormone (LH) secretion in ovariectomized ewes were examined over the course of 2 yr in relation to annual changes in environmental photoperiod, shifts in response to estradiol negative feedback control of LH secretion, and timing of the breeding season. Under natural environmental conditions, the frequency of LH pulses in individual ovariectomized ewes changed gradually and in close association with the annual cycle of day length. As days became shorter in late summer and autumn, LH pulse frequency increased; conversely, as day length increased in late winter and spring, frequency declined. Under artificial conditions in which ovariectomized ewes were exposed to different photoperiods, a similar inverse relationship was observed between day length and LH pulse frequency. The seasonal changes in frequency of LH pulses in ovariectomized ewes, although symmetric with the annual photoperiodic cycle, were not temporally coupled to the dramatic shifts in response to estradiol feedback inhibition of LH secretion at the transitions between breeding season and anestrus. The feedback shifts occurred abruptly and at times when LH pulse frequency in ovariectomized ewes was at, or near, the annual maximum or minimum. The tight coupling between LH pulse frequency and photoperiod leads to the conclusion that there is a photoperiodic drive to the LH pulse-generating system of the ewe. The temporal dissociation between changes in this photoperiodic drive and the seasonal shifts in response to estradiol negative feedback support the hypothesis that the neuroendocrine basis for these two phenomena is not one and the same.

Animals↗

PubMed1994

Effects of gonadal steroids on tonic luteinizing hormone (LH) release and luteinizing hormone-releasing hormone-induced LH release from bovine pituitary cells cultured in vitro.

The objective of this study was to investigate the direct effect of estradiol-17 beta (E2) and progesterone (P4) on LH release by pituitary cells of midluteal phase cows in vitro. Pituitaries were collected at the slaughterhouse; cells were dissociated with collagenase and hyaluronidase and maintained in a static culture system in Medium 199 (M199). Various concentrations of E2 (0.1-100 nM) and P4 (0.1 and 10 nM) were used to stimulate the cells for 2, 4, 6, 15, 24, 48, or 72 h. In addition, the synergistic action of E2 and P4 was investigated by exposure of the cells to a combination of the two hormones. At the end of each incubation, the cells were challenged with LHRH (1 nM) for 2 h. The medium was collected for LH analysis at the end of each incubation period and after the LHRH challenge; furthermore, intracellular LH content was quantified at the end of each experiment. The results indicate a positive action of E2 on basal release of LH beginning after 15 h of exposure (p < 0.01). LHRH-induced LH release was modulated by E2 in a time-dependent manner with an effect at first inhibitory, then stimulatory, and finally inhibitory again (p < 0.04). P4 alone did not affect LH release, but it negatively influenced LHRH-induced LH release. P4 also exerted a positive action on intracellular LH after 6 h of incubation. A substantial inhibitory effect (p < 0.001) on both tonic LH release and LHRH-induced LH release was observed in cells exposed for 16 h to P4 after a priming with E2 for 4 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Antiovulatory doses of antagonists of LH-RH inhibit LH and progesterone but not FSH and estradiol release.

The differential regulation of immunoactive FSH and LH secretion by endogenous LH-RH was studied using LH-RH antagonists (Ac-D-Trp1,2, D-Cpa2, D-Lys6, D-Ala10LH-RH (MI-1544) and (Ac-D-Nal1, D-Phe(pCl2), D- Trp3, D-Cit6, D-Ala10LH-RH (SB-030) in ovariectomized (OVX) and regularly cycling rats. Single injections of 10 micrograms and 100 micrograms doses and long-term treatment with 10 micrograms doses of MI-1544 were used in OVX animals. Serum and pituitary LH and FSH, as well as serum estradiol and progesterone was determined by RIA during and/or after the treatment. Single injections of MI-1544 in OVX animals caused prompt (in 2 h) and long-lasting (for more than 24 h) suppression of the serum LH, while no or late decrease (after more than 6 h) of the serum FSH. Long-term treatment with the same analog decreased the serum LH (by 50%) and moderately increased the pituitary LH (by 21%) but did not change the serum and the pituitary FSH concentrations. In normal rats, long-term treatment with both of our analogs also resulted in divergent alterations in the LH and FSH concentrations. Serum LH dropped to undetectable levels,while serum FSH did not change significantly. Pituitary LH increased (by 31 to 41%), while FSH decreased (by 27 to 38%). Marked depression was found in the serum progesterone (by 64%) but no significant change in the serum estradiol levels, after the long-term treatment for 21 days. The ovarian cycles were interrupted, and no ovulation appeared during the treatment. Significant decrease was detectable in the weight of the ovaries (by 46%), whereas the weight of the uteri did not change or slightly elevated (by 22%), after the treatment with SB-030 or MI-1544, respectively.

Amino Acid Sequence↗

PubMed1980

Plasma LH patterns after LHRH infusion in long-term, unanesthetized ovariectomized rats. Evidence for neural control of the pulsatile LH phenomenon.

Experiments were conducted in vivo to investigate further if the control of the pulsatile plasma LH phenomenon in ovariectomized (OVX) rats is located in the brain or in the adenohypophysis. Luteinizing hormone releasing hormone (LHRH) was infused at a constant rate (2--100 ng/h) through an indwelling venous cannula in unanesthetized, unrestrained OVX rats. Blood samples were collected at 5-min intervals through a second venous cannula prior to and during LHRH infusion for subsequent radioimmunoassay of plasma LH. LHRH infusion at 12.5, 50 and 100 ng/h did not interfere with the magnitude or the periodicity of LH pulses in plasma but the range within which plasma LH fluctuated was elevated. Phenobarbital (75 mg/kg BW; i.p.) blocked the pulsatile plasma LH and maintained the plasma LH nearly constant at reduced levels. Pulse i.v. injections of LHRH but not constant rate i.v. infusions restored pulsatile LH patterns in phenobarbital-treated OVX rats. The results are consistent with the view that pulsatile LHRH release is responsible for the pulsatile nature of plasma LH in OVX rats. The results do not support the concepts of a short-loop feedback of LH or an ultra-short-loop feedback of LHRH on LH secretion at least on an acute basis.

Animals↗

PubMed1976

Electrical stimulation of the arcuate nucleus in ovariectomized rats inhibits episodic luteinizing hormone (LH) release but excites LH release after estrogen priming.

The effect of electrical stimulation of the arcuate nucleus of the hypothalamus (ARH) on the blood levels of luteinizing hormone (LH) was studied in ovariectomized (ovx) rats. Unanesthetized, unrestrained rats were bled continuously (30 or 50 mul whole blood/4-6 min) through indwelling right atrial cannulae for 1 1/2-2h prior to the onset of stimulation. The bleeding was continued for the following three hours, during which electrical stimulation was applied for two 60 min periods separated by a 60 min non-stimulation period. Whole blood was analyzed for LH by radioimmunoassay. Electrical stimulation of the ARH in ovx rats inhibited the episodic LH release characteristic of these animals. The inhibition was rapid in onset, beginning within minutes, and lasted for most if not all of the stimulation period or longer. The blood LH levels returned to control values prior to the second stimulation period during which the inhibitory response was again seen. Stimulation in other hypothalamic areas outside the ARH was generally ineffective, although repeatable inhibition of episodic LH release did occur in 2 of 3 rats stimulated in the periventricular nucleus. In a second study, ovx rats were primed with 5 mug estradiol benzoate/100 g body weight/day for 2 days prior to stimulation. In these rats, stimulation of the ARH or median eminence produced increases in LH release, whereas stimulation in other hypothalamic areas outside the ARH was ineffective. The parameters of electrical stimulation that produced increases in LH release were the same as those that caused the inhibition of episodic LH release. The results demonstrate that electrical stimulation of the ARH inhibits LH release in ovx rats, but increases LH release if the animals have been primed with estrogen.

Animals↗

PubMed1994

Cells that express luteinizing hormone (LH) and follicle-stimulating hormone (FSH) beta-subunit messenger ribonucleic acids during the estrous cycle: the major contributors contain LH beta, FSH beta, and/or growth hormone.

There is a 2-fold increase in the percentage of gonadotropes bearing LH beta or FSH beta mRNAs or antigens as the cells approach proestrus. The purpose of this study was to identify the source of these cells with dual labeling techniques. The first hypothesis was that they stemmed from small monohormonal gonadotropes (containing only LH or FSH) that were driven to transcribe and translate the other gonadotropin. Alternatively, they may stem from other pituitary cell types. We detected the LH beta or FSH beta mRNAs by in situ hybridization (biotinylated oligonucleotide probes were detected by peroxidase-labeled avidin). Second, immunolabeling protocols localized the pituitary hormones. The percentages of cells with LH beta antigens and FSH beta mRNA increased to 81% of the LH beta antigen-bearing cells by the time of peak expression of FSH beta mRNA. Similarly, FSH beta antigen-bearing cells increased their expression of LH beta mRNA to 40% of such cells by the morning of proestrus. During the peak period of expression (the evening of proestrus), LH antigen-bearing cells had increased their expression of LH beta mRNA to 93%. Furthermore, 81% of the same cells expressed FSH beta mRNA. Thus, at least 80% of cells with LH antigens became bihormonal as the cells approached proestrus. This partially supports the first hypothesis for the origin of the new gonadotropes. However, the dual labeling studies also showed that 47% or 60% of cells with GH antigens expressed LH beta or FSH beta mRNAs, respectively, during peak expression (14% of pituitary cells contained gonadotropin mRNAs and GH antigens). Expression by cells with other antigens was low or absent (< 5% of pituitary cells). Perhaps a subset of somatotropes expresses gonadotropin mRNAs. Alternatively, the labeling could signify the presence of GH bound to GH receptors in gonadotropes. In either case, it appears that GH cells may be somehow linked to gonadotrope function as the cells approach proestrus.

Animals↗

PubMed1977

LH and FSH levels in urine and serum of prepubertal and pubertal children receiving a 3 hour infusion of LH-RH.

LH-RH was administered to 17 normal prepubertal and 14 pubertal children as well as to 6 GH deficient prepubertal patients. Urinary immunoreactive LH and FSH were measured in acetone extracts of 3 h collections prior to, during, and immediately after a 3 h infusion of 100 mug LH-RH. Peak LH excretion in response to LH-RH was higher in pubertal than prepubertal children. Girls excreted larger quantities of FSH after LH-RH than did boys. Serum LH and FSH increments evoked by LH-RH correlated significantly (P less than 0.01) with peak urinary gonadotropin excretion. These data suggest that measurement of urinary immunoreactive LH and FSH prior to and after LH-RH administration is clinically useful in evaluation of the reproductive endocrine system of young children and of individuals with low basal levels of gonadotropin.

Adolescent↗