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At least 127 records · Page 7Linked to original sources
PubMed1977

Immunoreactive LH-like substances in serum of hypophysectomized and prepubertal monkeys: inactive in an in vitro LH bioassay.

Serum LH levels in rhesus monkeys are commonly measured by a radioimmunoassay (RIA) utilizing ovine LH as the radioligand and a novel antiserum to ovine LH. Although meeting most criteria of validity, this RIA cross-reacts with serum from demonstrably hypophysectomized monkeys as well as serum from pre-pubertal monkeys. We have utilized the recently developed rat interstitial cell-testosterone assay (RICT) for measurement of serum LH in rhesus monkeys during various endocrine states and have compared the results with those obtained by RIA. The RICT in vitro bioassay was as sensitive, precise, and accurate as the RIA. Partially purified pituitary monkey LH preparations, varying by as much as 100-fold in purity, had similar potency estimates by both assays. The expected biphasic pattern of serum LH levels during the menstrual cycle as well as the usual increase in serum LH levels after ovariectomy was observed with both assays. In each case, however, basal serum LH levels were overestimated by the RIA and peak serum LH levels were underestimated by the RIA as compared to results obtained by the RICT bioassay. The most striking differences between the two assays were observed with serum from hypophysectomized and prepubertal monkeys. Whereas LH-like activity in such samples was high when measured by the RIA, it was undetectable by the RICT bioassay. The ratios of serum LH (RIA/RICT) varied from greater than 7.2 to greater than 17.4 in such sera. These results demonstrate the serious limitations of the ovine LH RIA for measurement of serum LH in rhesus monkeys. It appears that the RICT bioassay may be a suitable alternative method, especially in circumstances other than the menstrual cycle and after ovariectomy.

Animals↗
PubMed1985

Monosodium glutamate and pituitary gland luteinizing hormone (LH) release in response to LH-releasing hormone: an in vitro study.

We studied whether an increase in the basal LH release rate and/or the anterior pituitary gland (APG) LH response to LHRH is involved in maintaining normal or near-normal serum LH levels in monosodium L-glutamate (MSG)-treated rats which have small APGs for their body weight. Female rats were injected with MSG (4 mg/g BW) or saline on days 1, 3, 5, 7, and 9 after birth (day of birth = 0). At 8-9 weeks of age, saline-treated and MSG-treated rats were ovariectomized, and 7 days later, they were decapitated. Trunk blood was collected from 18 controls and 19 MSG-treated rats, and serum LH concentrations were measured by RIA. APGs were bisected and each hemi-APG was placed in culture medium for a 30-min preincubation period, followed by two 30-min incubation periods during which water or 10 or 30 ng LHRH were added to the medium. Despite the fact that the APGs of the MSG-treated rats were half the size of those of the saline-treated rats, the serum LH levels in the 2 groups were not different. Basal LH release rates (the response to water) and LHRH-induced LH release per mg APG were increased in MSG-treated rats. Calculation of the basal LH release rates and LHRH-induced LH release on the basis of the entire weights of the APGs showed no differences between the MSG-treated rats and the controls. In 6 additional control and 6 additional MSG-treated rats, the APG LH concentration was measured and was not different between the 2 groups. The results suggest that increases in both the basal LH release rate per mg APG and the amount of LH released per mg APG in response to LHRH are of importance in the maintenance of normal or near-normal serum LH concentrations in MSG-treated rats with small APGs.

Animals↗
PubMed1985

Effect of restricted nutrition on puberty in the lamb: patterns of tonic luteinizing hormone (LH) secretion and competency of the LH surge system.

The effects of undernutrition on the timing of puberty and regulation of LH secretion by the inhibitory and stimulatory feedback action of estradiol were examined in female sheep. The first experiment determined that maintenance of low BW (ca., 20 kg, four lambs) between 10 and 45 weeks of age prevented initiation of ovulation at the usual time (30 weeks of age). Ad libitum feeding of such growth-retarded lambs (n = 7) resulted in rapid catch-up growth and onset of reproductive cycles. The second experiment determined the effects of level of nutrition on tonic LH secretion in the presence and absence of inhibitory steroid feedback. Detailed LH patterns were obtained from agonadal lambs (ovariectomy at 20 weeks) that either remained undernourished (ca., 20 kg, 10-39 weeks of age) or were initially undernourished (10-27 weeks) and subsequently fed ad libitum (28-39 weeks). In undernourished lambs (n = 7), LH pulse frequency was slow, and only an occasional LH pulse was detected in the absence of steroid negative feedback; chronic treatment with low levels of estradiol (Silastic capsule), beginning at ovariectomy, prevented pulsatile LH secretion (six lambs). Ad libitum feeding (six lambs) produced a progressive severalfold increase in LH pulse frequency. Estradiol during ad libitum feeding (six lambs) markedly reduced amplitude of LH pulses and retarded the increase in LH pulse frequency. The third experiment, conducted at 40 weeks of age, determined the response to the stimulatory feedback action of estradiol. LH surges were readily induced in undernourished (20 kg) ovariectomized lambs (peak height 51 +/- 16 ng/ml, n = 6 of seven); chronic pretreatment with estradiol markedly reduced the magnitude of the LH surge (peak height 7 +/- 3 ng/ml, four of six). These findings raise the possibility that severe undernutrition prevents ovulation in the lamb by impairing the system governing GnRH secretion and its production of high-frequency LH pulses for follicular development to the preovulatory stage and its establishment of sufficient pituitary LH reserves for release by estradiol stimulatory feedback.

Aging↗
PubMed1989

Gonadotropin-releasing hormone-stimulated luteinizing hormone (LH) release from ovine gonadotrophs in culture is separate from phorbol ester-stimulated LH release.

The proposed involvement of protein kinase-C (PKC) as a mediator of GnRH action in pituitary cells was investigated. Treatment of dispersed ovine pituitary cells with the PKC activator phorbol 12-myristate-13-acetate (PMA) for 6 h at a dose of 10 nM stimulated the release of 5- to 10-fold more LH than did GnRH at the same dose. Analogs of PMA also stimulated LH release, but at levels parallel to their reported abilities to activate PKC. Treatment with GnRH plus PMA stimulated more LH release than either one alone in a strictly additive manner at all dose combinations from 10 pM to 100 nM. The PKC-activating diacylglycerol sn-1,2-dioctanoylglycerol also stimulated LH release that was additive with GnRH-stimulated LH release. Furthermore, retinal, an inhibitor of PKC, inhibited only PMA-stimulated LH release and not GnRH-stimulated LH release. These results do not support the theory that PKC activation is a necessary part of the mechanism of GnRH-stimulated LH release. The theory that calcium mobilization is also part of the mechanism of GnRH-stimulated LH release was, however, supported by the finding that GnRH did not stimulate LH release from ovine pituitary cells incubated in calcium-free medium. This demonstrates the absolute requirement for calcium in GnRH action, as proposed by others. In addition, the calcium ionophores A23187 and ionomycin were able to trigger LH release by themselves as well as augment GnRH- and PMA-stimulated LH release. This further strengthens the hypothesis that calcium mobilization is important in LH secretion.

Animals↗
PubMed1994

Effect of undernutrition on pulsatile luteinizing hormone (LH) secretion in castrate and intact male rats using an ultrasensitive immunofluorometric LH assay.

The recent development of an ultrasensitive immunofluorometric rat LH assay makes possible evaluation of pulsatile LH secretion in intact male rats under physiological conditions of minimal volume blood sampling without requiring orchidectomy. Specifically, we applied this assay to determine the effect of macronutrient restriction on pulsatile LH secretion in the presence or absence of testes. In testes-intact rats, halving of food intake for 7 days while maintaining micronutrient supply caused a reduction of mean, maximal, and basal LH levels and LH pulse amplitude (all P < 0.05) compared with those in ad libitum fed controls. The loss of body weight was positively correlated with decreases in mean LH level, pulse amplitude, and area under the curve (all P < 0.009). In contrast, the same food restriction in castrated rats caused an increase in pulse length and area under the curve and a decrease in pulse frequency, but did not change mean, maximal, and basal LH levels or LH pulse amplitude compared to castrated ad libitum fed controls (all P < 0.02). The observed positive correlations between body weight and the LH secretion parameters in intact rats were absent or reversed in castrated rats. This study demonstrates qualitatively different effects of macronutrient restriction on pulsatile LH secretion in castrated and intact rats, indicating that it is not necessary valid to extrapolate consequences of undernutrition on LH secretion from castrate to intact male rats. We conclude that undernutrition-induced inhibition of LH secretion involves both an indirect suppression of LH secretion via amplification of endogenous testicular negative feedback as well as more direct suppression of GnRH release.

Animal Nutritional Physiological Phenomena↗
PubMed1985

The changing ratio of bioactive to immunoreactive luteinizing hormone (LH) through puberty principally reflects changing LH radioimmunoassay dose-response characteristics.

The ratio (B/I) of bioactive to immunoreactive LH in plasma varies during pubertal maturation. To elucidate the basis for these changes, we compared the dose-response characteristics of LH standards to those of plasma LH before and after GnRH infusion in normal males at various pubertal stages and girls with Turner's syndrome. We used a human LH (hLH) RIA modified to optimize specificity for LH bioactivity by employing a hLH tracer maximally bioactive in the rat interstitial cell testosterone production (RICT) bioassay. The pituitary hLH standards LER-907, NHPP I-1, and NHPP I-2 were not parallel to one another in the RIA, but were parallel in the RICT. Their relative slopes in the RIA were 1:1.35:1.49, respectively. The B/I for immunoreactive LH in these standards were 1 (LER-907):3 (I-1):5 (I-2). Dose-response characteristics varied greatly by patient category in the RIA. In contrast to the RICT, in which plasma from all subject groups, except the prepubertal basal group, gave parallel dose-response slopes, the groups differed in the steepness of their plasma LH RIA dose-response curves in the following order: adult post-GnRH congruent to adult basal congruent to pubertal post-GnRH greater than pubertal basal congruent to prepubertal post-GnRH congruent to prepubertal basal greater than Turner's syndrome. Prepubertal basal samples most closely resembled LER-907 in dose-response characteristics, while adult samples were most similar to NHPP I-1 and I-2. These characteristics were not related to the absolute LH concentration. Although the RIA dose-response characteristics of plasma LH changed during puberty, the B/I of basal LH did not increase through puberty using the modified hLH RIA, although B/I still rose in GnRH-stimulated samples during puberty. Our data demonstrate that the principal cause of variability in B/I is the changing dose-response characteristics of plasma LH in the RIA. We suggest that the source of this variability is a change in the molecular characteristics of LH in different states of pubertal maturation and gonadal function. The results imply that better ways of assaying LH are needed.

Adolescent↗
PubMed1979

Studies on a protein synthesis dependent step in LH release by LH-RH.

The hypothesis that LH-RH induces LH release partly through a protein synthesis dependent step (protein factor) was further investigated using two different experimental designs. First, during incubation of pituitary glands of intact dioestrous female rats with a maximally active concentration of LH-RH, the inhibitor of protein synthesis cycloheximide was added at various times after the beginning of the incubation. The results show that it takes a relatively long time, i.e. more than 1 h of exposure to LH-RH before the amount of the protein factor has increased sufficiently to allow a maximal LH secretion. Secondly, LH-RH was injected iv after which the protein factor was assayed by incubating the pituitary glands with a maximally active concentration of LH-RH in the presence of cycloheximide and measuring LH release in vitro. It was found that 1 h after the injection sufficient protein factor was present to permit an elevated response to LH-RH. This response could be suppressed by injecting cycloheximide prior to LH-RH. When the interval between injection of LH-RH and beginning of the incubation was increased to 2 h, LH release in vitro decreased again. However, ovariectomy immediately before LH-RH injection resulted in maintenance of the elevated response toLH-RH in vitro, indicating a role of the ovaries in this phenomenon.

Animals↗
PubMed1975

Effect of intermittent infusion of LH-releasing hormone of serum LH and FSH levels in immature male rats.

The effect of intermittent intravenous infusions of LH-RH on serum LH and FSH levels was studied in immature male rats. At the end of the infusion, serum LH and FSH levels were higher than those after saline infusion. One hr after the end of infusion of LH-RH, serum LH levels fell, reaching saline control values, but FSH levels remained higher. Moreover, a pulsative pattern of LH release but not of FSH, was obtained during the intermittent infusion with LH-RH. These findings indicate that under appropriate conditions after administration of LH-RH, it is possible to find high GSH levels without a concomitant rise of LH levels. The continued elevation of FSH may be explained by the longer biological half-life of FSH. Estradiol benzoate depressed the basal serum GSH level and augmented the basal serum GSH level and augmented LH release after intermittent infusion with LH-RH, indicating that estrogen modified FSH/LH ratio. The results suggest that discordance of plasma LH and FSH levels which is occasionally observed in some physiological conditions does not necessarily indicate the presence of another FSH-RH which is distinct from LH-RH decapeptide.

Animals↗
PubMed1998

Decrease in the level and mRNA expression of LH-RH and EGF receptors after treatment with LH-RH antagonist cetrorelix in DU-145 prostate tumor xenografts in nude mice.

Using radioligand binding, RT-PCR, and Southern blot analyses, we evaluated whether agonist [D-Trp6]LH-RH and antagonist Cetrorelix could affect the levels of receptors for LH-RH and EGF and expression of mRNA for these receptors in DU-145 human androgen-independent prostate cancers xenografted into nude mice. Radioligand binding studies showed the presence of specific high affinity receptors for LH-RH and EGF in DU-145 prostate tumors. Cetrorelix, but not [D-Trp6]LH-RH significantly inhibited tumor growth. The concentration of LH-RH receptors was reduced by 22% (p<0. 05) and 67% (p<0.01) after 4 weeks of treatment with [D-Trp6]LH-RH and Cetrorelix respectively. The concentration of EGF receptors fell by 48% (p<0.05) in the [D-Trp6]LH-RH group, whereas Cetrorelix led to a 66% reduction (p<0.01). The expression of LH-RH and EGF receptor mRNA was investigated by RT-PCR analysis followed by Southern blotting. Densitometric analysis of the developed bands showed that the antagonist Cetrorelix decreased the expression of LH-RH receptor mRNA by 55% (p<0.01) compared to control group while the 20% reduction after treatment with the LH-RH agonist was non-significant. Treatment with [D-Trp6]LH-RH and Cetrorelix also reduced the expression of EGF receptor mRNA by 35% and 68% respectively (both, p<0.01) compared to control group. In conclusion, these data demonstrate that growth inhibition of DU-145 prostate tumors induced by prolonged administration of LH-RH antagonist Cetrorelix is accompanied by a marked decrease in the concentration of LH-RH and EGF receptors as well as in their mRNA levels.

Animals↗
PubMedDate not supplied

A radioimmunoassay system for LH based on the antigenic similitude of LH with HCG: methodology and applications.

A double antibody radioimmunoassay (RIA) system for LH (LH-IEP Kit) was developed using the antigenic similitude of LH with HCG. The first antibody (Ist Ab) is rabbit anti-HCG serum, initial dilution 1:200 000. The tracer is 125I-HCG (code MJ-14 Swierk Poland). The standard curve is calibrated with the reference preparation hLH-Ist-IRP 68/40 kindly offered by WHO. The IInd Ab is pig anti-rabbit IgG serum. The incubation conditions: volume-0.3 ml; time-24 hrs with Ist Ab and 24 hrs with the IInd Ab at ambient temperature. The sensitivity of the RIA system for LH is 1.5 mIU/ml. To validate our RIA system the LH was measured in the serum samples collected from 9 women during the menstrual cycles, from 2 boys during the GnRH test, from 2 amenorrheic women and from 20 children, adolescents and adults with miscellaneous pathologies. In all these samples, parallel measurements of LH and FSH were performed using DDR commercial RIA Kits-SSW. It is to be mentioned that the LH-RIA Kit-SSW is not completely homologous, the Ist Ab being rabbit serum anti-HCG. The results obtained during 4 menstrual cycles, in which the LH peak is observed around the mid point of the interval are: follicular phase 17.92 +/- 5.58 mIU/ml (means +/- SD) with LH-IEP-Kit and 5.51 +/- 2.77 mIU/ml with the LH-SSW-Kit, peak: 26.07 +/- 22.13 mIU/ml and 9.13 +/- 5.60 mIU/ml respectively; luteal phase: 12.55 +/- 5.46 mIU/ml and 3.4 +/- 2.38 mIU/ml, respectively. The LH values observed by the two kits through all 9 menstrual cycles are well correlated ("r" values in the range 0.7-0.9) but high discrepancies were observed in the remaining 3 cycles ("r" between 0.07 and 0.6). These discrepancies as well as those observed in some adolescents with genetic anomalies and in a patient at climacterium are suggesting that the two LH-RIA systems measure not only a common molecular area but also different areas of the LH circulating molecules.

Adolescent↗
PubMed1984

Effect of LH-RH on LH release from the dispersed pituitary cells of pregnant rats.

In order to study the mechanism which induces a sudden drop in serum LH levels between day 11 and 13 of pregnancy in rats, LH responses of the pituitary to LH-RH were investigated using an in vitro incubation system of the dispersed pituitary cells. Dispersed pituitary cells, obtained on day 10 or 15 of pregnancy, were incubated for 3 hours with synthetic LH-RH. The addition of 5ng LH-RH significantly increased the release of LH from the pituitary cells both on days 10 and 15 of pregnancy. The response of LH to LH-RH was significantly greater on day 10 than 15. A combination treatment of estradiol and progesterone blocked the stimulatory effect of LH-RH on LH release on day 10 but not on day 15. These results indicated that LH responsiveness of the pituitary was decreased between day 10 and day 15 of pregnancy, and this would play an important role in the lowering of serum LH levels during mid-pregnancy in rats. A possible role of progesterone and estradiol in the regulation of the responsiveness of the pituitary to LH-RH was also suggested.

Animals↗
PubMed1989

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

Plasma luteinizing hormone (LH) concentrations and the numerical density (Nv) 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 (Nv) of gonadal LH-binding cells in the maturation of the pituitary-gonadal axes of the chick embryo are discussed and evaluated.

Animals↗
PubMed1997

Expression of functional luteinizing hormone (LH) receptor and its messenger ribonucleic acid in bovine uterine veins: LH induction of cyclooxygenase and augmentation of prostaglandin production in bovine uterine veins.

We have previously reported that bovine endometrium contains LH/human CG binding receptors and LH induces cyclooxygenase and prostaglandin production in the bovine endometrium. The present study investigated 1) whether bovine uterine vein and artery contain LH receptor messenger RNA (mRNA) and receptor protein and 2) whether LH can regulate the formation of vasoactive eicosanoids by the uterine vein. The uterine vein endothelium, but not the uterine artery, contained LH receptor mRNA transcript essentially identical to that found in the bovine corpus luteum. The uterine vein endothelium also contained a 95-kDa immunoreactive receptor protein that bound to rat anti-LH receptor antibody in Western blots. The LH receptor mRNA and LH receptor were maximally expressed in the uterine vein from cows in proestrus/estrus compared with cows in luteal or postovulatory phases. Incubation of endothelial minces of uterine vein with LH resulted in a 2-fold increase in cyclooxygenase concentration as determined by Western blot using an antibody to ram seminal vesicle cyclooxygenase. The increase in cyclooxygenase was maximal in cows in proestrus/estrus compared with postovulatory and luteal phase cows. Incubation of proestrous/estrous uterine vein or artery minces with LH or mellitin (a phospholipase A2 stimulator) caused increased production of eicosanoids. In the uterine vein, LH caused a significant increase in both PGF2alpha (basal 4.1 +/- 0.4 vs. 5.7 +/- 0.4 ng/100 mg x 6 h, P < 0.01; N = 9 cows) and PGE2 (basal 5.7 +/- 0.3 vs. 7.7 +/- 0.8 ng/100 mg x 6 h, P < 0.01; N = 6 cows) but had no effect on prostaglandin production by the artery. Mellitin increased PGF2alpha production by both uterine vein and artery minces but had no effect on PGE2 production in either tissue. Addition of steroids (progesterone, estradiol) or cytokines (tumor necrosis factor-alpha, IL-6) to the uterine vascular tissues had essentially no effect on prostanoid production. In summary, bovine uterine vein from proestrous/estrous cows expressed the LH receptor and its mRNA. Expression of the receptor may have physiological significance as LH induces cyclooxygenase and increases prostaglandin release in the uterine vein. The maximal stimulation of the receptor and its mRNA at proestrus/ estrus may serve to increase the amounts of prostanoids reaching the regressing corpus luteum either directly by increasing prostanoid production or indirectly by increasing the blood flow to the ovary.

Animals↗
PubMed1990

Enhanced testosterone secretion in adult rams after establishment of a high-frequency, low-amplitude pattern of LH pulses in the nonbreeding season occurs without changes in the number or binding affinity of testicular LH receptors.

When the LH signal in the ram is changed from one of large and infrequent pulses to one of small and frequent pulses, the testes quickly become more responsive to LH and testosterone secretion is elevated, perhaps because the number and (or) binding affinity of testicular LH receptors have increased. An experiment was undertaken in the nonbreeding season (July) with 10 adult Dorset x Leicester x Suffolk rams that were about 3.5 years of age and 69 +/- 2 kg in body weight. Rams were given injections into the jugular vein of either 5 micrograms NIH-LH-S24 (in 1 ml saline) or vehicle every 80 min for 6 days. LH treatment produced a series of LH pulses that occurred three times more frequently and were 70% less in amplitude than pulses in the control rams, without causing mean LH concentration to increase. Endogenously produced LH pulses were not evident in the treated rams after LH injection began. The modified LH-pulse pattern elevated mean testosterone concentration by 150% (assessed on days 2 and 5), and caused the cumulative testosterone response to LH pulses, estimated by multiplying testosterone-pulse amplitude by frequency per 6 h, to increase progressively by 180% (days -2 through 5). Enhanced testicular steroidogenic activity, presumably due to greater enzymatic activity and cholesterol availability within Leydig cells, was not associated with increases in either the concentration or affinity of LH-binding sites in the testis (assessed on days 3 and 6).

Animals↗
PubMed1992

Blockade of the LH response induced by the agonist D-Trp-6-LHRH in rats by a highly potent LH-RH antagonist SB-75.

During treatment of prostate cancer patients with luteinizing hormone-releasing hormone agonist, a transient LH and sex steroid release, which precedes the secretion blockade, may result in a flare-up of the disease, whereas the antagonists induce an immediate suppression. The administration of the modern, superactive LHRH antagonist SB-75 before or together with the agonist D-Trp-6-LHRH should prevent the "flare-up" phenomena. In order to demonstrate that the LHRH antagonist can prevent the initial stimulation of gonadotropins in response to LHRH agonists, groups of 5-7 male rats were injected s.c. with the antagonist SB-75 in doses in 100, 500, and 1,000 micrograms/rat 1 hour prior to or 1, 2, and 3 days before administration of D-Trp-6-LHRH agonist (50 micrograms/rat). Supraphysiological doses of the agonist were used in order to obtain prolonged stimulation of LH release, which was necessary to study the duration and the extent of LH release inhibition. Blood samples were taken before and 2, 6, 24, 48, and 72 hours after D-Trp-6-LHRH stimulation for measurement of LH levels. The administration of SB-75 in doses of 500 and 1,000 micrograms/rat 3 days prior to administration of the agonist significantly lowered LH response (P less than 0.01), as compared to animals injected with D-Trp-6-LHRH alone. The D-Trp-6-LHRH-stimulated LH secretion was markedly more suppressed by all 3 doses of the antagonist in rats pretreated with SB-75 2 days prior to the stimulation with the agonist. An even greater reduction in LH response could be observed in rats injected with SB-75 1 day prior to the agonist, the magnitude of LH response being decreased by 75% with 500 micrograms/rat SB-75 and by 90% with 1 mg/rat SB-75. The LH response was virtually abolished when the antagonist, SB-75 was given in doses of 500 or 1,000 micrograms/rat 1 hour prior to the D-Trp-6-LHRH injection. Under these conditions, the agonist-induced LH and testosterone secretion was completely suppressed during the whole period of the experiment. The antagonist to agonist dose ratio of 2 to 1 produced a 90% decrease in the LH response to D-Trp-6-LHRH at 2 hours and 75% at 5 hours after agonist administration. The effects of LHRH decapeptide itself (500 micrograms/rat) on LH secretion could be totally suppressed by an injection of 50 micrograms/rat of SB-75 1 hour beforehand.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMedDate not supplied

LH-RH-dependent synthesis of protein necessary for LH release from rat pituitary glands in vitro.

Anterior pituitary glands of intact diestrous and gonadectomized female rats were incubated with a supramaximally active dose of LH-RH. Puromycin (P) and cycloheximide (C) did not consistently affect the LH release from glands of ovariectomized rats. In intact rats, LH release induced by LH-RH occurred in two phases, an initial one (relatively slow rate of release) and a secondary one (high rate of release). P and C had no effect on the initial phase, but prevented the secondary one. Pre-incubation with LH-RH prevented the effect of P and C added after 4 hours. Since P and C did not affect the total amount of LH present in media and hypophyses, the LH-released during the P- and C-sensitive phase is not newly formed LH. It is concluded that LH-RH induces the synthesis of protein which is necessary for LH-RH-induced LH release. The initial phase of LH release is made possible by protein already present in the glands at the beginning of the experiment.

Animals↗
PubMed1980

Competition of various LH--RH analogs and fragments with 135I-LH--RH for specific binding sites on isolated pituitary plasma membranes.

The displacement by various LH--RH analogs and fragments of 125I-LH--RH specifically bound to plasma membranes isolated from rat anterior pituitaries was investigated. The addition of increasing amounts of unlabelled LH--RH resulted in an increasing displacement of bound 125I-LH--RH. When some fragments of LH--RH or of an analog with little biological activities were incubated, a much weaker affinity for LH--RH binding sites could be observed. No correlation between biological effectiveness and binding affinity was, however, found when several highly active LH--RH analogs were tested. The potent analogs competed much less efficiently for specific binding sites on isolated plasma membranes than LH--RH. Binding experiments with iodine-labelled (D-Ser(But)6-LH--RH(1--9)-nonapeptide-ethylamide indicated that the small binding affinity of the superactive analog may be due to a lower association rate while the dissociation rate is comparable to that of LH--RH. Contrary to LH--RH, no binding equilibrium was reached during 2 h of incubation of the analog with plasma membranes. The physiological role of LH--RH binding sites on isolated pituitary plasma membranes remains to be elucidated.

Animals↗
PubMed1985

Serum luteinizing hormone-releasing hormone (LH-RH) and gonadotropic hormones in men after a bolus dose of LH-RH: comparison of different doses and routes of administration.

Serum levels of luteinizing hormone-releasing hormone (LH-RH), LH, and follicle-stimulating hormone (FSH) were measured for 60 minutes after 5- and 20-micrograms bolus doses of LH-RH given either intravenously or subcutaneously to 20 healthy men, for the study of LH-RH pharmacokinetics and the corresponding pituitary gonadotropin release. Intravenous (5- and 20-micrograms) LH-RH administration revealed much sharper LH-RH pulses, with significantly higher levels between 1 and 5 minutes (P less than 0.001) but lower levels between 30 and 60 minutes (P less than 0.05), compared with the subcutaneous route. No statistically significant differences were observed in the magnitude and time occurrence of maximum LH release or in the area under the LH response curves between intravenous and subcutaneous LH-RH administration, either in the 5-micrograms or in the 20-micrograms group. FSH responses were small and insignificant in all the performed tests. The intravenous route of administration seems preferential in therapeutic regimens that use pulsatile exogenous LH-RH, because the conditions of intermittent pituitary stimulation are more adequately fulfilled and the risk of dose accumulation is reduced. Furthermore, LH-RH doses of 5 micrograms are capable of producing adequate pituitary LH release, whereas increases in the pulse dose up to 20 micrograms seem to have no additional effects.

Adult↗