Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “LH”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 109 records · Page 6Linked to original sources
PubMed1978

Temporal changes in medial basal hypothalamic LH-RH correlated with plasma LH during the rat estrous cycle and following electrochemical stimulation of the medial preoptic area in pentobarbital-treated proestrous rats.

In the present studies we have simultaneously measured changes in medial basal hypothalamic (MBH) leutenizing hormone-releasing hormone (LH-RH) and in plasma LH by radioimmunoassay in female rats at various hours during the 4-day estrous cycle and under experimental conditions known to alter pituitary LH secretion. In groups of rats decapitated at 12.00 h and 15.00 h on estrus and diestrus, plasma LH remained at basal levels (5-8 ng/ml) and MBH-LH-RH concentrations showed average steady state concentrations of 2231 +/- 205 pg/mg. On the day of proestrus hourly measurements of MBH-LH-RH between 12.00 h and 21.00 h suggested rhythmic rises and falls in the decapeptide concomitant with rises and falls in plasma LH. In a second group of pentobarbital-anesthetized proestrous rats a significant decline in MBH-LH-RH occurred (to 573 +/- 137 pg/mg) which then remained at low concentrations between 14.00 h and 18.00 h proestrus. Following bilateral preoptic area (MPOA) electrochemical stimulation of pentobarbital-treated proestrous rats, LH was significantly increased by 30 min, peaked between 90-120 min and returned to basal levels by 210 min poststimulation. In the same animals within 15 min poststimulation, MBH-LH-RH increased from the basal concentrations noted after pentobarbital anesthesia to elevated levels comparable to those observed throughout estrus, diestrus and on proestrous morning. Further, as plasma LH rose to peak concentrations and declined to basal plasma values, rhythmic rises and falls in MBH-LH-RH were observed with intervals between pulses of approximately 60 min. Seemingly, hypothalamic LH-RH is released as pulsatile pulses from a releasable pool; this pool is replenished and again LH-RH is discharged in response to constant stimulation by the preoptic brain.

Animals↗
PubMed1984

Comparison between the biological effects of LH-RH and buserelin on the induction of LH release from hemi-pituitary glands of female rats in vitro.

The biological effects of LH-RH and the agonist [D-Ser(But)6-des Gly10]-LH-RH(1-9)-ethylamide (buserelin) were compared during 8 h of incubation with female rat hemi-pituitary glands. Similar dose-response relationships were found for LH-RH and buserelin as concerns the release of luteinizing hormone (LH) by pituitary glands from intact and ovariectomized rats. Also the LH secretion patterns from glands of intact rats were similar: an initial low response was followed by a fast increase (priming effect) after which the response declined again (desensitization). In a subsequent experiment pituitary glands from ovariectomized rats were first exposed to LH-RH or buserelin for 4 h and then further incubated in medium only. After discontinuation of the stimuli the rate of LH release decreased in all cases, but this decrease was significantly greater when the glands had been exposed to LH-RH. Short-term (1/2, 1 or 2 h) exposures to LH-RH or buserelin followed by an intervening period (1 1/2, 1 or 0 h, respectively) of incubation in medium only resulted in an almost similar, significant increase in the subsequent protein synthesis-independent LH response to LH-RH (priming effect). Only preincubation with LH-RH for 2 h was significantly more effective. The results demonstrate equal intrinsic activities for LH-RH and buserelin. Differences in the biopotencies for LH-RH and buserelin in vivo and in vitro may occur only after discontinuation of the external stimuli.

Animals↗
PubMed2002

Changes in subcellular distribution of pituitary receptors for luteinizing hormone-releasing hormone (LH-RH) after treatment with the LH-RH antagonist cetrorelix.

Treatment with antagonists of luteinizing hormone-releasing hormone (LH-RH) leads to down-regulation of pituitary LH-RH receptors. Thus, the effect of LH-RH antagonists is similar to that of the LH-RH agonists, but the mode of action of antagonists is not completely understood. The aim of this study was to investigate the effects of LH-RH antagonist cetrorelix on the binding characteristics and subcellular localization of receptors for LH-RH in rat pituitaries. Radioligand binding studies, performed after in vitro desaturation, revealed that a single s.c. injection of cetrorelix at a dose of 100 microg per rat significantly decreased the number of pituitary membrane receptors for LH-RH in a time-dependent manner with the nadir occurring at 6 h. In contrast, 2-6 h after cetrorelix treatment, the concentration of binding sites for LH-RH in the nuclei of rat pituitaries was significantly higher (P < 0.01) than in controls. Chronic administration of cetrorelix also decreased the level of membrane receptors for LH-RH by 83% (P < 0.01) after 7 days, and 86% (P < 0.01) after 14 days. The number of LH-RH binding sites in the nuclear pellet was increased 3-fold (P < 0.01) by days 7 and 14 after the initiation of treatment with cetrorelix. A single injection or prolonged treatment with LH-RH antagonist also decreased the mRNA expression of pituitary receptors for LH-RH. Our results demonstrate that the down-regulation of LH-RH receptors on the cell membranes of rat pituitaries after therapy with antagonist cetrorelix is associated with an increase in receptor concentration in the nuclei. These phenomena could be related to the internalization and subcellular translocation of LH-RH receptors.

Animals↗
PubMed1991

Preponderance of basic isoforms of serum luteinizing hormone (LH) is associated with the high bio/immune ratio of LH in healthy women and in women with polycystic ovarian disease.

In an attempt to correlate serum LH isoform distribution with its bio/immuno ratio, follicular phase blood samples from four normally cycling women and four patients with polycystic ovarian disease (PCOD) were studied. Chromatofocusing of peripheral serum samples across a pH gradient of 9.5-4.5 yielded a broad area of LH immunoreactivity comprising several peaks in the pH range of 7.2-9.0, and six other major peaks at pH values of 9.4, 6.8, 6.4, 5.1, 4.7 and less than 4.0. In addition, the bioactive and immunoreactive levels of LH were measured in the unfractionated serum samples. In three out of four PCOD patients and one healthy woman, the majority of LH species (approximately 70%) were distributed at a pI value greater than 7.0. All of them had a high bio/immuno ratio (greater than 2.0) and an elevated bioactive level of serum LH (greater than 40 IU/l). Conversely, fewer alkaline pI isoforms of LH were found in the other three normal women and one PCOD patient, who had low levels of the bio/immuno ratio of LH (less than 2.0) and bioactive LH (less than 40 IU/l). A significant (P less than 0.05) direct correlation was observed between the bio/immuno ratio of serum LH and the proportion of alkaline LH eluted. In conclusion, as demonstrated previously in the pituitary, the bio/immuno ratio of serum LH also correlates well with the charge distribution of LH isoforms. The results indicate that an altered isoform distribution with more basic LH forms is associated with a high biological activity of serum LH.

Biological Assay↗
PubMed1976

Effect of a new LH-RH analogue (D-Ser(TBU)6-EA10-LH-RH) on gonadotrophin and gonadal steroid secretion in men.

The effect of a new analogue of the gonadotrophin-releasing hormone LH-RH, D-Ser(TBU)6-EA10-LH-RH, on the secretion of LH, FSH, as well as testosterone, oestradiol, HGH, prolactin, TSH, and cortisol was studied in normal men. The same subjects were injected intravenously in 4-day intervals with 1.0, 2.5, 5.0, and 10.0 mug of this substance. A significant LH but no FSH release was seen after doses of 1.0 and 2.5 mug LH-RH analogue, while after 5.0 and 10.0 mug dose-dependent increases of LH and imposed elevations of FSH were observed. Peak levels of LH were reached after 30 min, those of FSH after intravenous injection after 120 min. LH and FSH remained elevated for 8-10 h. LH peak levels after 5 mug of LH-RH analogue were comparable to those seen after injection of 100 mug of the decapeptide LH-RH. Following the release of LH and FSH after doses of 5.0 and 10.0 mug LH-RH analogue, there was a late stimulating effect in testosterone and oestradiol secretion. HGH, TSH, prolactin, and cortisol were not influenced by the LH-RH analogue.

Adult↗
PubMed1986

Progesterone and LH variations after LH-RH administration in the luteal phase of the menstrual cycle.

We have investigated the pituitary and luteal responses to LH-RH and their related changes. 11 normal women were studied during the luteal phase (day +4/+11). Blood samples were collected every 15 min for a basal period of 180 and 120 min after the intravenous administration of 25 micrograms of LH-RH. Progesterone (P) and LH were assayed by radioimmunoassay. Data were analyzed as maximum peak and its percent increase (delta max), integrated secretory area (ISA) and percent increase of ISA (delta A) in respect to basal values for both P and LH. LH-RH elicited a secretory response of both hormones in all cases. ISA of LH was significantly greater after LH-RH administration in respect to basal values (p less than 0.001) and delta max accounted to 475 +/- (SE) 36% of the basal concentration. Luteal responsiveness varied from about 115-130% to more marked increments. ISA of P differed from basal to stimulated conditions (p less than 0.05) and delta max was 166 +/- (SE) 14%. The analysis of temporal relationship between P and LH secretion showed that LH promptly rose after LH-RH, while the enhancement of P plasma levels occurred within 31 +/- 19 min after LH rise. Then P levels reached a plateau, values of which were statistically different from those observed before LH-RH administration. In two cases where luteal function was blunted or absent, in spite of marked increments of LH, P secretion did not occur. These data are consistent with the presence of close relationships between hypothalamic, pituitary and luteal functions and strengthen the contention about the usefulness of LH-RH during luteal phase for the lifespan and maintenance of corpus luteum.

Adult↗
PubMed1992

Oxytocin/neurophysin-I messenger ribonucleic acid in bovine granulosa cells increases after the luteinizing hormone (LH) surge and is stimulated by LH in vitro.

Bovine granulosa cells express the oxytocin/neurophysin-I (OT/NP-I) gene and secrete OT in vitro. We have shown previously that bovine granulosa cells isolated from the preovulatory follicle after the LH surge secrete 20 times more OT over 5 days in culture than granulosa cells obtained before the surge. LH or FSH stimulates OT secretion in vitro by granulosa cells isolated before the LH surge. We also observed that granulosa cells of preovulatory follicles isolated before the LH surge respond to OT with an increase in progesterone secretion, suggesting that OT may be involved in regulating the follicular/luteal phase shift, or ovulation, in an autocrine fashion. The objective of this study was to determine whether the increase in OT secretion from granulosa cells after the LH surge is regulated at the level of mRNA accumulation, peptide synthesis, and/or peptide secretion. Bovine preovulatory follicles were obtained during the early follicular phase (approximately 36 h before the LH surge), during the midfollicular phase (approximately 12 h before the LH surge), or during the late follicular phase (after the LH surge). Total RNA isolated from granulosa cells and theca interna at the time of cell isolation or after culture with or without LH was subjected to Northern analysis for OT/NP-I mRNA and quantified by densitometry. OT/NP-I mRNA was not detectable or was barely detectable in granulosa cells collected during the early or midfollicular phase (n = 6 and n = 4 follicles, respectively), but a strong hybridization signal was obtained from RNA isolated after the LH surge (n = 5 follicles; P < 0.01). In contrast, OT/NP-I mRNA was not detectable in theca interna before or after the LH surge. Although OT/NP-I mRNA was not detectable in granulosa cells isolated 24 h after prostaglandin F2 alpha injection, after 24 h in culture, a weak OT/NP-I mRNA hybridization signal was observed in RNA from granulosa cells in LH-containing cultures. After 72 h in culture, granulosa cells cultured in control, as well as in LH-containing medium, exhibited a strong signal for OT/NP-I mRNA, but granulosa cells treated with LH exhibited a stronger OT/NP-I hybridization signal than control cultures (P < 0.01). Theca interna did not yield any OT/NP-I hybridization signal initially, and none was induced in culture.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Cholecystokinin (CCK)-induced stimulation of luteinizing hormone (LH) secretion in adult male rhesus monkeys: examination of the role of CCK in nutritional regulation of LH secretion.

Studies were performed with the overall goal of testing the hypothesis that cholecystokinin (CCK), a peptide hormone released from the gastrointestinal tract in response to meal consumption, provides a metabolic signal which modulates LH secretion in response to changes in the body's nutritional intake. In an initial study to document the effects of CCK on LH secretion in adult male rhesus monkeys, sulfated CCK-8 (7 and 15 micrograms/kg) was administered to six monkeys, and blood samples were collected from indwelling venous catheters. The 15-micrograms/kg dose of CCK elicited a rapid release of LH, with peak LH levels of 31.29 +/- 7.19 ng/ml occurring within 5-15 min. To determine the CCK receptor type mediating the effect of CCK on LH secretion, specific CCK type-A (L-364,718) and type-B (L-365,260) receptor antagonists (1 mg/kg) were administered to five monkeys 15 min before CCK administration. The CCK-A antagonist completely blocked LH secretion in response to CCK, whereas the CCK-B antagonist had no effect. To assess whether endogenous CCK, released in response to food intake, stimulates LH secretion, six monkeys were fasted for 1 day and then provided with a normal meal of monkey chow (i.e. a refeed meal) the following day, with either no antagonist, CCK-A antagonist, or CCK-B antagonist administered 30 min before the meal. As previously demonstrated, meal consumption after a brief period of fasting caused a rapid stimulation of pulsatile LH secretion. The refeed meal led to a comparable stimulation of LH secretion regardless of whether monkeys received no antagonist (3.7 +/- 0.44 LH pulses/9 h), CCK-A antagonist (3.33 +/- 0.56 LH pulses/9 h), or CCK-B antagonist (4.0 +/- 0.78 LH pulses/9 h). These results indicate that CCK can stimulate LH secretion in adult male rhesus monkeys, acting via type-A CCK receptors. However, endogenous CCK released in response to meal intake does not appear to be responsible for the meal-induced stimulation of LH secretion that occurs when monkeys are fed a normal meal after a brief period of fasting.

Animal Feed↗
PubMed1990

Persistence of concordant luteinizing hormone (LH), testosterone, and alpha-subunit pulses after LH-releasing hormone antagonist administration in normal men.

LHRH antagonists suppress pituitary and gonadal function by competing with endogenous LHRH for binding to gonadotroph receptors. To determine the mechanism of suppression of gonadotropin secretion we studied the effects of a single dose of a LHRH antagonist on the pulsatile activity of serum bioactive LH (Bio-LH), immunoreactive LH (IR-LH), alpha-subunit, and testosterone for 24 h in normal men. The LHRH antagonist, Nal-Glu [( Ac-D2Nal1,D4ClPhe2,D3Pal3,Arg5,DGlu6-(AA), DAla10]LHRH) was given as a single sc injection of 5 mg to five normal men. Blood samples were collected every 10 min during a 10-h baseline period and for 14 h after administration of the antagonist. IR-LH, alpha-subunit, and testosterone were measured in triplicate, and Bio-LH in duplicate. Pulses were then evaluated using Cluster analysis; all replicates were entered in the pulse analysis. After administration of the Nal-Glu antagonist, IR-LH levels decreased (P less than 0.001) from 2.81 +/- 0.06 at baseline to a nadir of 0.75 +/- 0.02 U/L. Bio-LH levels followed the same pattern, decreasing by 89% (P less than 0.001) from 4.54 +/- 0.13 to a nadir of 0.51 +/- 0.13 U/L 6.8 h after the injection of Nal-Glu. In contrast, serum alpha-subunit levels did not change (P greater than 0.05) during the 14-h period after antagonist administration (0.85 +/- 0.01 and 0.75 +/- 0.01 microgram/L before and after Nal-Glu, respectively). Serum testosterone levels decreased by more than 80%, from 17.6 +/- 0.2 at baseline to a mean nadir of 3.3 +/- 0.7 nmol/L 12.8 h after Nal-Glu administration. Pulse frequency and the number of significant pulses remained the same for all of the measured hormones during the 10-h baseline period and the 14 h after Nal-Glu administration. In contrast, the pulse amplitude of IR-LH, Bio-LH, and testosterone decreased significantly after injection of the antagonist. The pulse amplitude of the alpha-subunit also declined, albeit not significantly. Coincidence analysis revealed that during both the 10-h baseline and the 14-h post-Nal-Glu period there was a highly significant (P less than 10(-5) nonrandom synchrony between peaks of IR-LH, Bio-LH, alpha-subunit, and testosterone. These results suggest that coordinate pulsatile secretion of IR-LH, Bio-LH, and testosterone persists after the administration of 5 mg Nal-Glu LHRH antagonist.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗
PubMed1993

Estradiol amplifies the amount of luteinizing hormone (LH) secreted in response to increasing doses of gonadotropin-releasing hormone by specifically augmenting the duration of evoked LH secretory events and hence their mass.

Amplification of LH release during the preovulatory LH surge could result from increased GnRH secretion and/or estradiol's facilitation of the dose-dependent actions of GnRH. We have investigated the mechanisms of estrogen's enhancement of GnRH action by evaluating LH release in response to four consecutive iv doses of GnRH (7.5, 25, 75, and 250 ng/kg) administered in randomized order followed by a fifth (maximal) dose of 750 ng/kg GnRH. The GnRH dose-response study was carried out before and after 10 days of estradiol treatment (0.2 mg/day percutaneously) in nine healthy postmenopausal women. Deconvolution analysis was used to quantitate specific measures of GnRH-stimulated LH secretion as well as estimate the half-life of endogenous LH. We found that 10 days of estradiol delivery did not alter the calculated half-life of immunoradiometric LH (126 +/- 10 min basally vs. 135 +/- 14 min during estrogen), but amplified the total mass of LH secreted in response to the five doses of GnRH; viz. 201 +/- 29 (control) vs. 406 +/- 58 IU/L (estrogen) (P < 0.001). Estradiol specifically enhanced the maximal value of the GnRH dose-LH secretory response curve; viz. from a mass of LH secreted of 46 (41-51) IU/L (basal) vs. 113 (93-139) IU/L (estrogen) (P < 0.001). Estradiol did not induce a significant leftward shift of the GnRH dose-LH secretory response curve, since the half-maximally effective dose of GnRH (ED50) was 9 (3.6-18) (control) vs. 19 (10-31) ng/kg (estradiol). The increased mass of LH secreted in the estrogen-rich milieu was due to a doubling of LH secretory burst duration, with no change in amplitude. We conclude that amplified LH secretory burst duration constitutes a novel neuroendocrine mechanism by which estradiol can promote GnRH self-priming of LH release by the previously estrogen-deprived human anterior pituitary gland in vivo.

Analysis of Variance↗
PubMed1975

Response of serum LH, FSH and prolactin to injection of synthetic LH-RH into rat anterior pituitary.

Changes in serum LH, FSH and prolactin were measured by radioimmunoassay following injection of synthetic LH-RH into the anterior pituitary and median eminence of rats. The time course of serum levels of LH and FSH after injection of synthetic LH-RH into the pituitary showed a peak at 15 min. The synthetic LH-RH had a more marked releasing effect on LH than on FSH. After injection of 20 ng into the pituitary, the serum LH rose to about 10.7 times the control level but the serum FSH only to about 1.8 times. A significant rise of serum LH over the control level was noted after injection of more than 0.2 ng of synthetic LH-RH, while that of serum FSH was after injection of more than 2 ng. An injection of 2 ng of synthetic LH-RH into the pituitary following 0.1 mug of estradiol benzoate resulted in a fall of serum LH and FSH levels, and a rise of serum prolactin level. An injection of 2 ng of synthetic LH-RH into the median eminence resulted in a tendency towards slight decrease in serum LH and FSH. No significant response of serum prolactin to synthetic LH-RH was noted.

Animals↗
PubMed2003

Effects of pregnancy on pulsatile secretion of LH and gonadotrophin-releasing hormone-induced LH release in sheep: a longitudinal study.

Pulsatile LH secretion and its control throughout pregnancy have not been fully determined in sheep. Expt 1 determined the patterns of LH secretion in five ewes on days 10, 20, 60 and 120 of pregnancy and on day 10 postpartum, compared with those on day 10 of the oestrous cycle. Mean (+/- SEM) concentrations of LH declined steadily throughout pregnancy (ANOVA, P < 0.01) and were lower (P < 0.01) on day 60 (0.19 +/- 0.3 ng ml(-1)) and on day 120 (0.18 +/- 0.4 ng ml(-1)) of pregnancy than on day 10 of the oestrous cycle (0.55 +/- 0.04 ng ml(-1)). This decrease was due to a significant reduction in the number and the amplitude of LH pulses. Only on day 120 of pregnancy were progesterone concentrations higher (P < 0.01) than on day 10 of the oestrous cycle. Although concentrations of progesterone on day 10 postpartum were barely detectable, mean LH concentration (0.45 +/- 0.09 ng ml(-1)) was not different from that on day 10 of the oestrous cycle. Expt 2 examined the LH responses in a separate group of four ewes to a physiological dose of GnRH (0.2 microg) on days 10, 20, 60 and 120 of pregnancy and on day 10 postpartum, compared with those on day 10 of the oestrous cycle. The area under the LH response curve and the maximum LH concentrations induced by GnRH declined steadily throughout pregnancy (ANOVA, P < 0.01) and were lower (P < 0.01) on days 60 and 120 of pregnancy than on day 10 of the oestrous cycle, but these parameters were not different between day 10 postpartum and day 10 of the oestrous cycle. Expt 3 examined the LH responses in a separate group of four ewes to a potent GnRH agonist, buserelin (0.5 microg), on days 10, 60 and 120 of pregnancy. The area under the LH response curve and the maximum LH concentrations induced by GnRH were lower (P < 0.01) on days 60 and 120 than on day 10 of pregnancy, but were not different between days 60 and 120. This longitudinal study demonstrates that the pulsatile LH release and pituitary responsiveness to GnRH decreases progressively as pregnancy advances, but does not support the hypothesis that high concentrations of progesterone are solely responsible for the inhibition of pulsatile LH secretion and GnRH-induced LH release during pregnancy in sheep.

Animals↗
PubMed1997

The rotational diffusion of LH receptors differs when receptors are occupied by hCG versus LH and is increased by cytochalasin D.

We have examined the rotational diffusion of the luteinizing hormone (LH) receptors binding human chorionic gonadotropin (hCG) or ovine luteinizing hormone (oLH) in MA-10 Leydig tumor cells using time-resolved phosphorescence anisotropy techniques. LH receptors binding erythrosin isothiocyanate (ErITC)-derivatized oLH were rotationally mobile with rotational correlation times of 62 micros, 48 micros, 38 micros, and 29 micros at 4 degrees C, 15 degrees C, 25 degrees C, and 37 degrees C, respectively. ErITC-hCG bound to the LH receptor was rotationally immobile, showing no anisotropy decay at 4 degrees C, 15 degrees C, 25 degrees C, and 37 degrees C. To determine whether cytoskeletal components influenced the rotational diffusion of LH receptors, we measured rotational diffusion of LH receptors on MA-10 cells treated with 20 microg/ml cytochalasin D and on plasma membrane preparations. Following 1 h exposure to cytochalasin D, the rotational correlation times for hCG-occupied LH receptors were typically 11 micros at 37 degrees C compared to > 1000 micros on untreated cells. Treatment of MA-10 cells with cytochalasin B or colchicine had no affect on LH receptor rotational diffusion. Rotational correlation times for LH-occupied receptors decreased from 29 micros to 12 micros at 37 degrees C following cytochalasin D treatment. The rotational diffusion of LH receptors on plasma membrane preparations was similar to that observed for LH- and hCG-occupied receptors on intact cells treated with cytochalasin D. These various results indicate that there are differential effects of LH and hCG binding on the interactions of LH receptors with plasma membrane proteins and that microfilaments anchor the hCG- and LH-occupied receptors.

Actin Cytoskeleton↗
PubMed1994

A single injection of a gonadotropin-releasing hormone (GnRH) antagonist (Cetrorelix) postpones the luteinizing hormone (LH) surge: further evidence for the role of GnRH during the LH surge.

OBJECTIVES: To assess the ability of a new third-generation GnRH antagonist, Cetrorelix (Asta Medica AG, Frankfurt am Main, Germany), to postpone the LH surge after a single injection during the late follicular phase. DESIGN: A single 5-mg (group 1, n = 7) or 3-mg (group 2, n = 3) dose SC of Cetrorelix was administered during the late follicular phase, on the day of the cycle when plasma E2 exceeded 150 pg/mL (550 pmol/L). Estradiol, LH, FSH, and P levels were measured daily from day 5 of the cycle until day 10 after antagonist administration. Transvaginal ultrasonographies were performed on the day of injection and after antagonist treatment. SUBJECTS: Ten normal women with regular ovulatory menstrual cycles. RESULTS: In group 1, Cetrorelix was administered on day 14.6 +/- 5 (mean +/- SD) of the cycle, when the mean plasma E2 level was 181 +/- 32 pg/mL (664 +/- 117 pmol/L) (mean +/- SD). Plasma LH and FSH decreased by 56% +/- 19% and 29.5% +/- 16% (mean +/- SD), respectively, reaching the nadir 24 hours after Cetrorelix administration. Estradiol decreased by 85% +/- 17%, reaching the nadir 48 hours after antagonist injection. In group 2, Cetrorelix was administered on day 14.3 +/- 1.2 of the cycle when the mean plasma E2 level was 169 +/- 21 pg/mL (618 +/- 77 pmol/L). Plasma LH and FSH decreased by 66% +/- 18% and 32% +/- 6%, respectively, reaching a nadir 24 hours after Cetrorelix administration. Estradiol decreased by 81% +/- 9%, reaching the nadir 24 to 48 hours after antagonist administration. The LH surge was interrupted in every case. In six of seven subjects from group 1, the LH surge was delayed, occurring 6 to 17 days after the antagonist injection. In the remaining woman, Cetrorelix was administered at the beginning of the LH surge (LH = 13 IU/L): the LH level fell immediately by 54%, and the surge was postponed by 3 days. In group 2, in three of three subjects, the LH surge was delayed, occurring 6 to 9 days after the antagonist injection. No adverse effects were observed, except for very slight and transient erythema and pruritus at the injection site. CONCLUSION: Cetrorelix is a very potent new GnRH antagonist. A single injection during the late follicular phase delays the LH surge, even if the latter has already begun. In addition, this new-generation GnRH antagonist is very well tolerated and simple to use. Our data reinforce the role of GnRH during the LH surge and point to a role for new GnRH antagonists in controlled ovarian hyperstimulation to avoid premature LH surges and subsequent luteinization.

Adult↗
PubMed1999

Correlation between LH response to challenges with GNRH and naloxone during lactation, and LH secretion and follicular development after weaning in the sows.

The aim of this study was of establishing a correlation between endogenous LH secretion and the magnitude of the LH response to challenges with GnRH and the opioid antagonist naloxone during lactation, and between these characteristics and LH secretion and follicular development after weaning. Sows (n = 9) were sampled for 6 h at day 2 post-partum, for 12 h on day 26 of lactation and for 6 h immediately after weaning at day 27 of lactation. Four hours after the beginning of sampling at day 26 of lactation all sows were injected with 2 mg/kg i.v. of naloxone hydrochloride and 5 h later with 100 microg/sow of GnRH. Follicular development was studied in all sows at slaughter the day after weaning. There was an effect of time (sampling period; P < 0.001) on mean plasma LH, with an increase (P < 0.05) in LH the day after weaning compared to mean LH concentrations during lactation. Naloxone and GnRH treatment both increased (P < 0.05) mean LH concentrations. A positive relationship (r = 0.58, P < 0.01) between mean plasma LH after GnRH and after weaning was established. Although there were differences (P < 0.001) between sows in follicular fluid volume, there were no correlations between mean follicular fluid volume and mean LH concentrations after GnRH or after weaning. These data indicate that the LH response to GnRH during late lactation could be useful predictor of LH activity after weaning. However, none of the measures of endogenous or induced LH secretion were associated with differences in ovarian follicular size after weaning. Direct evidence is therefore still needed for a functional link between differences in LH in lactation and differences in fertility after weaning.

Animals↗
PubMed1999

Exogenous luteinizing hormone (LH) increases estradiol response patterns in poor responders with low serum LH concentrations.

PURPOSE: Our purpose was to investigate whether the addition of exogenous leuteinizing hormone (LH) increases estradiol secretion in LH-depleted women undergoing controlled ovarian hyperstimulation (COH) with purified follicle stimulating hormone (FSH). METHODS: We carried out case series and retrospective analysis of midfollicular serum LH concentrations and estradiol response patterns in COH cycles. All patients initially received gonadotropins containing purified FSH. Human menopausal gonadotropin containing LH was added to poor responders with low midfollicular LH concentrations. RESULTS: The addition of exogenous LH to the COH regimen significantly increased estradiol secretion in poor responders with low midfollicular endogenous LH concentrations. This was confirmed statistically by an average change in the slope of the estradiol patterns from 27.54 to 85.49 after the addition of exogenous LH. Furthermore, patients with midfollicular serum LH concentrations < 3.0 mIU/ml had significantly lower midfollicular and peak estradiol (E2) concentrations compared to patients with LH concentrations > or = 3.0 mIU/ml (352.3 and 2094.3 vs 855.6 and 3757.1 pg/ml, respectively). CONCLUSIONS: The addition of exogenous LH increases E2 response patterns in poor responders with low midfollicular serum LH concentrations. Low midfollicular serum LH concentrations are associated with significantly lower midfollicular and peak E2 concentrations.

Adult↗
PubMed1986

Regulation of expression of genes for light-harvesting antenna proteins LH-I and LH-II; reaction center polypeptides RC-L, RC-M, and RC-H; and enzymes of bacteriochlorophyll and carotenoid biosynthesis in Rhodobacter capsulatus by light and oxygen.

RNA levels were measured by blot hybridization to study the coordinate and differential expression of Rhodobacter capsulatus genes for light-harvesting I antenna proteins LH-I and LH-II; reaction center (RC) polypeptides L, M, and H; and bacteriochlorophyll and carotenoid biosynthesis in response to light and O2. The genes for LH-II alpha and beta subunits only have one transcript, 0.5 kilobase (kb) long, whereas the genes for LH-I have two transcripts (0.5 and 2.6 kb). The small transcript (0.5 kb) is the mRNA only for LH-I beta and alpha polypeptides, whereas the large transcript (2.6 kb) codes for RC-L, RC-M, and the beta and alpha polypeptides of LH-I, as well as the product of an unknown open reading frame designated ORF C2397. These five genes thus comprise a single operon (designated the puf operon). The mRNA specifying the LH-II polypeptides is more abundant, more sensitive to changes in O2 concentration, and shows a variation over a wider range than that of the mRNA for LH-I, indicating that the genes for LH-II and LH-I/RC are regulated independently. The gene for RC-H (puhA) has at least two transcripts (1.2 and 1.4 kb) that initiate within ORF F1696 and respond differentially to light intensity. The expression of the genes coding for RC-L, RC-M, and RC-H is coordinately regulated by light intensity and O2 concentration. An increase in light intensity causes a decrease in the expression of the genes for LH-I, LH-II, and RC proteins. The genes coding for the enzymes in the bacteriochlorophyll biosynthetic pathways are regulated by light intensity and O2 in a manner similar to that of the genes for LH and RC proteins. The crt genes coding for the enzymes in carotenoid biosynthetic pathways, however, are regulated in an opposite fashion: high light intensity results in increased expression of crt genes. These results are interpreted based on the protective function of carotenoids under high light intensity in the presence of O2.

Bacterial Proteins↗
PubMed1980

Biphasic fluctuation of pituitary responsiveness to LH-RH during the rat estrous cycle. Role of endogenous LH-RH and ovarian steroids in its modulation.

The role of the endogenous LH-RH and gonadal steroids on the fluctuation of the pituitary responsiveness to an analog of LH-RH in rats was studied. A specific sheep serum against LH-RH and a superactive analog of LH-RH [D-Ala6,desGly-NH2(10)]LH-RH ethylamide, which does not cross-react with the LH-RH antiserum, were used. In control animals, the pituitary response to 400 ng of LH-RH varied during the estrous cycle, the greatest responses being on the days of proestrus (P) and estrus (E) and the lowest on diestrus I (DI) and diestrus II (DII). A similar pattern was observed in the same animals when 10 ng of [D-Ala6,desGly-NH2(10)]LH-RH ethylamide were used. In animals treated with anti-LH-RH serum, the LH response to the analog was greater than that in control rats on day I (DI) and day 2 (DII) and was smaller on day 3 (P) and on day 4 (E). The magnitude of the pituitary responsiveness to the analog in animals treated or not with the anti-LH-RH serum depended to some extent on the serum progesterone/estradiol ratio. The antiserum against LH-RH lowered the high serum levels of estradiol which are normally seen on P and E but not of progesterone. This indicates that a possible extraovarian source of progesterone exists, possibly from the adrenals. In conclusion, the cycling fluctuation of the plasma progesterone/estrogen ratio in the female rat could act at the pituitary level to modify LH-RH action.

Animals↗