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PubMed1986

[The effect of synthetic chicken LH-RH on the release of LH and FSH and ovulation in rats (a comparative study of synthetic mammalian LH-RH and chicken LH-RH)].

Recently, Miyamoto et al and King et al, independently isolated chicken LH-RH and determined its chemical structure as [Gln8] LH-RH. In this report, the in vivo effect of synthetic chicken LH-RH on the release of LH and FSH and ovulation in rats was investigated. A single i.v. injection of chicken LH-RH, as well as mammalian LH-RH, induced a significant increase of plasma LH levels at 15 min after injection in adult male rats. Plasma LH levels then declined at 30 min to 60 min and returned to basal levels at 120 min. The biological potency of chicken LH-RH estimated from plasma LH levels at 15 min after injection in adult male rats by parallel line assay was 4.1% of that of mammalian LH-RH. It was likely that the activity of chicken LH was shorter in duration on the LH secretion as compared with that of mammalian LH-RH because of quickly decreased plasma LH levels. Plasma FSH levels were also increased, but the increment of FSH was not so obvious as compared with that of LH. Plasma FSH levels reached a plateau at 15 min and did not return to basal levels at 120 min in either the chicken LH-RH injection groups or the mammalian LH-RH injection groups. The chicken LH-RH was able to induce an increase of plasma LH and FSH and ovulation in pentobarbital-blocked, proestrous female rats. The biological potency of chicken LH-RH estimated from plasma LH levels at 15 min after injection in pentobarbital-blocked, proestrous female rats was 2.2% that of mammalian LH-RH. The ovulation-inducing potency of chicken LH-RH estimated from ED50 was about 2.1% of that of mammalian LH-RH. It is noteworthy that chicken LH-RH has a LH and FSH releasing and ovulation inducing-activity on rats in vivo, but its biological potency is weaker and of shorter duration compared with that of mammalian LH-RH, although the chemical structure of chicken LH-RH is different from that of mammalian LH-RH.

Animals↗

PubMed1994

Cooperation between LH-RH and LH in the direct action on the ovary: LH-RH stimulation of LH/hCG receptors, basal and LH-induced cAMP and cGMP release by porcine granulosa cells in vitro.

LH-RH effects on LH/hCG receptors content, on basal and LH-stimulated cAMP and cGMP release by cultured porcine granulosa cells, were investigated by radioreceptor analysis and radioimmunoassay. It was found that LH-RH additions (10, 100, 1000 or 10,000 ng/ml medium) increased the number of LH/hCG binding sites in granulosa cells. LH or hCG (0.1, 1, 10 or 100 ng/ml) increased both cAMP and cGMP secretion by the cell culture. LH-RH alone (0.1, 1, 10, 100 or 1000 ng/ml) had the same stimulating effect on both cyclic nucleotides. The addition of LH-RH (100 ng/ml) to the medium supplemented with LH (10, 100, 1000, 10,000 or 100,000 ng/ml) enhanced LH-stimulated cAMP and cGMP output from the culture. The present observations suggest that LH-RH can act as synergist of LH and of hCG increasing a number of LH/hCG receptors and stimulating basal and LH-induced cyclic nucleotide release by ovarian cells.

Animals↗

PubMed1997

Differential responses in anterior pituitary luteinizing hormone (LH) content and LH beta- and alpha-subunit mRNA, and plasma concentrations of LH and testosterone, in bulls treated with the LH-releasing hormone agonist deslorelin.

Anterior pituitary gland contents of LH and LH beta- and alpha-subunit mRNAs, and circulating concentrations of LH and testosterone, were determined in bulls treated with the LH-releasing hormone (LHRH) agonist deslorelin. Brahman (Bos indicus) bulls (14-month-old) were allocated to two groups and received the following: Control (n = 5), no treatment; Deslorelin (n = 4), four deslorelin implants (approximately 200 micrograms total deslorelin/day) for 36 d. Plasma concentrations of LH were higher in bulls treated with deslorelin on Day 1, had returned to typical levels by Day 8, and did not differ for control bulls and bulls treated with deslorelin from Day 8 to Day 29. Pituitary content of LH on Day 36 was reduced (P < 0.001) in bulls treated with deslorelin (33 +/- 4 ng/mg) compared with control bulls (553 +/- 142 ng/mg). Relative pituitary content of LH beta-subunit mRNA was also reduced on Day 36 in bulls treated with deslorelin (Control, 0.65 +/- 0.10; Deslorelin, 0.22 +/- 0.04; P = 0.003). However, alpha-subunit mRNA relative content did not differ (Control, 0.73 +/- 0.15; Deslorelin, 1.06 +/- 0.12; P > 0.05). Plasma concentrations of testosterone were increased over the period of the experiment in the bulls treated with deslorelin compared with control bulls. This is the first demonstration of reduced pituitary content of LH beta-subunit mRNA and LH, and unaltered content of alpha-subunit mRNA, in bulls treated with LHRH agonist. This was associated with apparently typical plasma concentrations of LH and elevated plasma testosterone. The anterior pituitary in bulls treated with LHRH agonist, therefore, undergoes classical desensitization and downregulation, but plasma LH and testosterone are not suppressed.

Animals↗

PubMed1984

Blockade of LH and FSH secretion by LH-releasing hormone, by the LH-releasing hormone analogue, buserelin, and by combined treatment with LH-releasing hormone and oestradiol benzoate.

The LH and FSH release-stimulating (experiment 1) and -blocking (experiment 2) effects of LH-releasing hormone (LHRH) and of the LHRH analogue D-Ser(But)6-des-Gly10-LHRH-ethylamide (buserelin), as well as the effect of combined treatment with LHRH and oestradiol benzoate (OB; experiment 3) on the 'supra-maximally' LHRH-stimulated release of LH and FSH were studied in rats ovariectomized for 2 weeks. Pretreatment with LHRH (250 or 500 ng/h) or buserelin (250 ng/h) for 6 days was effected by means of subcutaneously implanted Alzet osmotic minipumps; control rats received a 'sham pump', i.e. a piece of silicone elastomer with the dimensions of a minipump. Oestradiol benzoate (3 micrograms/injection) or solvent was injected subcutaneously 75 and 27 h before the induction of LH/FSH responses. Experiment 1 revealed that after infusion of LHRH and buserelin, both at the rate of 1 microgram/h, plasma LHRH concentrations were established which were about twice as low as the plasma buserelin concentrations. This might suggest that buserelin has a longer half-life than LHRH. As an LH and FSH release-stimulating substance, however, it appeared that buserelin was about as effective as LHRH. Experiment 2, however, suggested that as an LH/FSH release-blocking agent buserelin was much more effective than LHRH. In addition, after buserelin pretreatment the pituitary glands contained much less LH and FSH than after LHRH pretreatment at both dose levels used.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

The dynamics of LH-induced desensitization of adenylate cyclase and LH receptor internalization in rat Leydig cells at physiological levels of LH.

The LH-induced desensitization of adenylate cyclase and LH receptor internalization in rat Leydig cells in vitro has been investigated using sub-physiological to pharmacological concentrations of LH. Leydig cells pretreated with LH for 1 h in the presence of a phosphodiesterase inhibitor showed a dose-dependent decrease in the subsequent response to a high dose of LH; this was significant with concentrations of greater than 350 fmol/l. The maximum amount of desensitization was 60%. The time-course of LH-induced desensitization of the adenylate cyclase system was investigated; with 3 nmol LH/l cyclic AMP was increased in a linear manner up to 45 min, after which time there was either no further production or (with the higher concentrations) a decreased rate of production. In order to determine whether the 'non-desensitized' adenylate cyclase activity was dependent upon LH, the LH-treated cells were acid-washed to remove residual LH; cyclic AMP production still continued, albeit at a lower rate, thus indicating that this adenylate cyclase activity did not require the further presence of LH. The effect of various concentrations of LH on the level of surface-associated LH receptors was determined in the presence of monensin to prevent receptor recycling. A dose- and time-dependent decrease was found; this was significant after 2 h with 3.5 pmol LH/l and reached a maximum of 63% of the control with 3.5 nmol/l. A dose- and time-dependent reversal of desensitization occurred if the cells pretreated with LH were washed and reincubated; with 35 pmol LH/l and after 2 h the cells were fully responsive to a challenge with fresh LH. With higher concentrations of LH in the pretreatment, partial or no recovery was found. These studies demonstrate that physiological and sub-physiological concentrations of LH induce a rapid desensitization of Leydig cell adenylate cyclase. Internalization of occupied and unoccupied LH receptors also occurred. It is proposed that these two events are linked and may, paradoxically, and because of the low numbers of LH receptors, be necessary to maintain the normal response of Leydig cells to LH in vivo.

Adenylyl Cyclases↗

PubMed2001

Luteinizing hormone-releasing hormone (LH-RH) antagonist Cetrorelix down-regulates the mRNA expression of pituitary receptors for LH-RH by counteracting the stimulatory effect of endogenous LH-RH.

The mechanisms through which LH-RH antagonists suppress gonadotroph functions and LH-RH receptor (LH-RH-R) production are incompletely understood. To elucidate these mechanisms, we investigated the effects of Cetrorelix on the mRNA expression of pituitary LH-RH-R and luteinizing hormone (LH) secretion in three experimental systems with different pituitary LH-RH environments. Ovariectomy induced 3.61-fold and 6.34-fold increases in the mRNA expression of pituitary LH-RH-R in rats after 11 and 21 days, respectively. After (5 h) a single injection of 100 microg Cetrorelix, no significant decrease occurred in the mRNA levels of pituitary LH-RH-R in ovariectomized (OVX) rats with high pituitary exposure to LH-RH, but there was a significant 23.2% reduction in cycling rats with normal hypophysial LH-RH environment. Prolonged treatment for 10 days with a Cetrorelix depot formulation releasing 100 microg/day decreased the concentration of mRNA for pituitary LH-RH-R by 72.6% in OVX rats, but only by 32.9% in normal rats. The decline in serum LH was 98.7% in OVX rats and 63.2% in normal rats, resulting in a minimal 0.1--0.2 ng/ml LH concentration in both groups. A continuous exposure of pituitary cells to 100 nM Cetrorelix in the superfusion system, which is devoid of LH-RH, did not cause any significant changes in LH-RH-R mRNA level. These studies demonstrate that prolonged exposure to Cetrorelix in vivo, but not in vitro, down-regulates the mRNA expression of the pituitary receptors for LH-RH. Our findings indicate that LH-RH antagonists exert their inhibitory effects on the gene expression of pituitary LH-RH-R by counteracting the stimulatory effect of endogenous LH-RH.

Animals↗

PubMed1986

Effects of two kinds of chicken luteinizing hormone-releasing hormone (LH-RH), mammalian LH-RH and its analogs on the release of LH and FSH in Japanese quail and chicken.

A newly isolated and characterized chicken luteinizing hormone-releasing hormone-II (chicken LH-RH-II, Miyamoto et al., 1984) had luteinizing hormone (LH) and follicle-stimulating hormone (FSH) releasing activity in vitro and in vivo in Japanese quail: the activity was almost equal to chicken LH-RH-I and mammalian LH-RH. These three LH-RHs induced the release of LH several times higher than that of FSH in vitro and also in vivo. No significant difference between chicken LH-RH-I and LH-RH-II was observed in LH releasing activity in vitro using chicken pituitary gland in the same incubating condition as in quail. Another experiment indicated that no synergism existed between chicken LH-RH-I and -II and that there was neither LH nor FSH releasing activity in [D-Phe2, Pro3, D-Phe6]-LH-RH or in mesotocin. However, the same potency as in the chicken LH-RH-II was observed in [D-Ala6, des-Gly10]-LH-RH ethylamide, a superactive analog in mammals. The results indicate that an avian adenohypophysis differs from a mammalian adenohypophysis in its responsiveness to LH-RH suggesting that an avian LH-RH receptor may have a lower specificity in "recognition" of LH-RH molecules than a mammalian LH-RH receptor has.

Animals↗

PubMed1994

Follicular development, oocyte viability and recovery in relation to follicular steroids, prolactin and glycosaminoglycans throughout the estrous period in superovulated heifers with a normal LH surge, no detectable LH surge, and progestin inhibition of LH surge.

Estrous cycles of heifers (n = 137) were synchronized with prostaglandin (PGF2 alpha) and follicular development stimulated with follicle stimulating hormone. Twenty-eight animals were administered Norgestomet implants 12 hr prior to the initial PGF2 alpha injection to suppress the LH surge that initiates ovulation. Animals were ovariectomized every 12 hr after the initial PGF2 alpha (7-9/time, 12-108 hr and at 192 and 240 hr post PGF2 alpha) and divided into three treatment groups to consist of: 1) animals exhibiting a normal luteinizing hormone (LH) surge (n = 86), 2) animals in which no LH surge was detected (n = 23), and 3) suppression of the LH surge via Norgestomet implants (72-108 hr, n = 28). Follicular diameter was measured and follicular fluid was collected for analysis of prolactin, estradiol, progesterone and glycosaminoglycan concentrations. Progesterone concentrations were increased in animals exhibiting an LH surge as compared to animals in which no LH surge was detected; primarily in large follicles (> 8 mm diameter) after the LH surge. Animals not exhibiting an LH surge also had increased follicular progesterone concentrations compared to Norgestomet-implanted animals (242.3 +/- 36.3 vs 86.7 +/- 6.4 ng/ml, respectively, P < .01), indicating some LH stimulation. Follicular estradiol in animals exhibiting an LH surge increased up to the time of LH surge detection and then declined whereas animals with no LH surge detected had follicular estradiol concentrations that declined after the PGF2 alpha injection. No differences were noted between those that did not exhibit an LH surge or in which the LH surge was suppressed with Norgestomet in relation to follicular estradiol concentrations. Follicular estradiol concentrations increased with follicular size in all treatment groups (P < .01). Follicular concentrations of prolactin were increased in small follicles (P < .05; < or = 4 mm diameter) and follicular prolactin increased from 12 to 36 hr post PGF2 alpha injection, then declined after the LH surge. Follicular glycosaminoglycan concentrations decreased with increases in follicular size (P < .01) and were higher in animals that did not exhibit an LH surge (P < .01). No differences in follicular glycosaminoglycans were noted between Norgestomet-implanted animals and those not exhibiting an LH surge. In the animals representing days 4 and 6 of the subsequent estrous cycle (192 and 240 hr post PGF2 alpha), numbers of small-sized follicles were increased. Follicular progesterone and estradiol concentrations were related to atretic large follicles unovulated from the prior estrus and a new wave of growth in small and medium follicles.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Gonadotrophin releasing hormone agonist suppressive treatment of ovarian function decreases serum LH-beta and bioactive LH but maintains elevated levels of LH-alpha.

Ten patients with endometriosis were treated by a continuous subcutaneous infusion of the GnRH agonist buserelin for 6 months. Although serum oestradiol decreased into the menopausal range within 2 weeks after starting treatment, serum LH levels as measured by immunoassay remained elevated at least fivefold over baseline during the entire treatment. However, the bioactivity of LH as determined by mouse Leydig cell assay was rapidly lost, changing the mean +/- SEM bioactivity/immunoassay ratio from 2.4 +/- 0.5 before treatment to 0.4 +/- 0.01 after only 1 week of medication. When LH-alpha and LH-beta immunoreactivities were assessed by specific antibodies, the serum LH-alpha profile was parallel to immunoreactive LH whereas the LH-beta profile corresponded to the pattern of bioactive LH. LH-alpha was elevated at least tenfold over baseline whereas LH-beta decreased to less than 35% of pretreatment level. The alpha/beta ratio shifted from 1.3 +/- 0.2 before treatment to 0.04 +/- 0.06 after 2 weeks of buserelin infusion. Thus in response to continuous buserelin exposure, the gonadotrophin releases excessive amounts of LH having predominant LH-alpha immunoreactivity. The effective loss of LH bioactivity would be related to decreased LH-beta subunits. The significance of high levels of LH-alpha subunits. The significance of high levels of LH-alpha or possibly modified LH molecules remains to be evaluated during GnRH agonist treatment using well characterized assays.

Adult↗

PubMed1975

The effect of oral and vaginal administration of synthetic LH-RH and [D-ALA-6, DES GLY-10-NH2]-LH-RH ethylamide on serum LH levels in ovariectomized, steroid blocked rats.

Effects of oral and vaginal administration of LH-RH and [D-ALa-6, DesGly-10-NH2i1-LH-RH ethylamide (D-Ala-6-LH-RH-EA) on serum LH levels in ovariectomized, estrogen, progesterone treated rats were investigated. Oral administration of synthetic LH-RH induced a quick rise of serum LH levels with the greatest elevation at 15 min at any dose levels tested. On the other hand, oral administration of D-Ala-6-LH-RH-EA resulted in a slow but progressive rise of LH during 120 min of observation. The total amount of LH released by 10 mug of the analog was much greater than the total released by 1000 mug of LH-RH. Vaginal administration of 100 mug of LH-RH mixed with Carbowax induced a progressive rise of LHwhich was indistinguishable from that following 10 mug of the analogue, suggesting that the potency of the analogue is 10 times greater than that of LH-RH for vaginal administration. Ten mug of LH-RH given through the vagina induced a rapid rise of LH with the peak at 15 min, whereas 1 mug of the analog induced a slow but progressive rise. Greater resistance of D-Ala-6-LH-RH-EA than LH-RH against in vivo breakdown is postulated as one of the causes of greater and prolonged LH release by the former.

Administration, Oral↗

PubMed1975

Parellel inhibition of LH-RH-induced cyclic AMP accumulation and LH and FSH release by LH-RH antagonists in vitro.

The relative potencies of seven antagonists of LH-RH to inhibit LH-RH-induced cyclic AMP accumulation and LH and FSH release were measured using rat hemipituitaries in vitro. At appropriate concentrations, [Des-His2, D-Ala6] LH-RH, [Des-His2, D-Ala6, des-Gly-NH210] LH-RH ethylamide, [Des-His2, D-Leu6] LH-RH, [D-Phe2] LH-RH, [Des-His2, Des-Gly-NH210] LH-RH propylamide, [D-Phe2, D-Leu6] LH-RH and [D-Phe2, D-Phe6] LH-RH led to parallel inhibition of cyclic AMP accumulation and LH and FSH release. [D-Phe2, D-Leu6] LH-RH and [D-Phe2, D-Phe6] LH-RH can inhibit 50% of LH-RH action at molar ratios of 100 and 30, respectively. These findings of parallel changes of cyclic AMP levels and LH and FSH release add strong support to the already obtained evidence for a mediator role of the adenylate cyclase system in the action of LH-RH in the anterior pituitary gland.

Animals↗

PubMed1988

Divergent effects of the antiestrogen tamoxifen and of estrogens on luteinizing hormone (LH) pulse frequency, but not on basal LH levels and LH pulse amplitude in men.

We studied the role of estrogens on LH pulse modulation in men in two ways. Firstly, we compared LH pulse frequency and amplitude in 13 normal men before and after 6 weeks administration of the antiestrogen tamoxifen (10 mg twice daily). Secondly, we compared LH pulse frequency and amplitude between a group of 10 agonadal men not receiving sex steroid treatment and a group of 9 agonadal men (male to female transsexuals) continuously treated with 50 micrograms ethinyl estradiol/day. Tamoxifen administration to normal men resulted in a significant rise in the mean serum LH level from 5.7 +/- 1.3 (+/- SD) to 10.1 +/- 2.4 U/L, which was associated with significant increases in LH pulse frequency (from 4.2 +/- 1.5 to 5.8 +/- 1.7/7 h) and LH pulse amplitude (from 3.8 +/- 0.9 to 4.6 +/- 0.7 U/L). In the group of agonadal men the mean LH pulse frequency was 6.8 +/- 1.5/7 h, while it was 5.9 +/- 1.7/7 h in the estrogen-treated agonadal group (P = NS). The mean serum LH level and LH pulse amplitude were, however, significantly lower in the estrogen-treated agonadal men than in the agonadal men (14.7 +/- 7.0 vs. 34.3 +/- 8.6 and 4.1 +/- 1.8 vs. 7.4 +/- 1.8 U/L, respectively). We conclude that estrogens reduce basal LH levels and LH pulse amplitude. With regard to the modulation of LH pulse frequency our data provide contradictory results. While an antiestrogen increased LH pulse frequency in normal men, estrogen alone produced no change in LH pulse frequency in agonadal men. The study design in the agonadal men ignores the possible interaction of the two major testicular hormones (estradiol and testosterone) on gonadotropin secretion. Therefore, a possible explanation for this discrepancy in the effects of antiestrogen and estrogen could be an interaction between estrogens and androgens on gonadotropin secretion at the level of the LHRH pulse generator.

Adult↗

PubMedDate not supplied

Temporal changes in FSH and LH concentrations following the administration of a potent LH-RH inhibitory analogue ( [N-Ac-D-Trp1, 3, D-p-Cl-Phe2, D-Phe6, D-Ala10]-LH-RH) to oophorectomized rhesus monkeys.

A series of studies was performed in order to assess the antigonadotropic potency of an inhibitory analogue of LH-RH (IA-LH-RH) ( [N-Ac-D-Trp1, 3, D-p-Cl-Phe2, D-Phe6, D-Ala10]-LH-RH) in oophorectomized rhesus monkeys. I) Single administration of 1 mg IA-LH-RH im resulted in a prompt and significant decrease of serum levels of FSH and LH which lasted for at least 24 h. A specific rebound of serum LH to higher concentrations than baseline occurred in all animals at +48 or +72 h. II) Exogenous LH-RH at a dose of 150 micrograms was administered iv 2 or 18 h after the injection of 1 mg IA-LH-RH. Blood was drawn at 0, 10, 20, 30, 60, 120 and 180 min post LH-RH. The rise in LH and FSH levels observed in the control animals was not altered when LH-RH was administered 2 h after the antagonist, but it was significantly inhibited and delayed when LH-RH was given 18 h after the LH-RH inhibitory analogue. These results show that antagonistic analogues of LH-RH are potent inhibitors of gonadotropin concentrations in non-human primates. Their potential use in conditions in which inhibition of gonadotropin secretion and/or release is desired is discussed.

Animals↗

PubMed1991

Mediation of the short-loop negative feedback of luteinizing hormone (LH) on LH-releasing hormone release by melatonin-induced inhibition of LH release from the pars tuberalis.

The pineal hormone melatonin is thought to mediate the effects of the pineal gland on seasonal reproduction by altering the release of gonadotropins. The mechanism by which melatonin controls gonadotropin secretion has been obscure. Recently, labeled 2-iodomelatonin was used to localize melatonin receptors in brain by radioautography. The highest concentration of melatonin receptors was found in the pars tuberalis of the pituitary gland of mammals. Pituitary hormones, in particular luteinizing hormone (LH), have been localized in cells of the pars tuberalis. Consequently, we hypothesized that melatonin might act on its receptors in the pars tuberalis to alter the release of LH. It would then be possible for this LH to diffuse into the overlying median eminence, there to alter the release of LH-releasing hormone (LHRH) from the axons of the LHRH neurons. To evaluate this hypothesis, we incubated median eminence-pars tuberalis tissue from male rats in vitro. After preincubation in Krebs-Ringer bicarbonate buffer for 30 min, test substances were added to fresh medium and the incubation was continued for 30 min. LHRH or LH released into the medium was measured by radioimmunoassay. Melatonin induced a dose-related release of LHRH with the maximum response at the greatest concentration tested (1 microM). This concentration of melatonin also significantly reduced the release of LH into the medium. The increased release of LHRH induced by melatonin (10 microM) was completely blocked by the addition of LH (50 ng/ml), which by itself had no significant effect on LHRH release. Rat LH antiserum (final dilution, 1:1800) significantly elevated LHRH output, whereas normal rabbit serum at a similar dilution had no effect. Finally, LHRH (0.1 microM) induced a significant release of LH from median eminence-pars tuberalis tissue that was completely blocked by melatonin (10 microM). The results support the hypothesis that LH released from the pars tuberalis diffuses to the LHRH terminals in the median eminence to suppress LHRH release. Melatonin acts on its receptors in the pars tuberalis to inhibit LH release, thereby stimulating the release of LHRH from its terminals in the median eminence. The negative short-loop feedback of LH inhibits basal LHRH release in vitro since antiserum against LH increased LHRH release. The results suggest a concept concerning the mechanism by which melatonin can affect the release of pituitary hormones from the pars tuberalis. It is likely that these pituitary hormones diffuse into the median eminence to modify the release of hypothalamic releasing and inhibiting peptides, thereby altering plasma pituitary hormone concentrations.

Animals↗

PubMed1978

Effect of steroids in combination with LH-RH on the release of LH and FSH in LH-RH-primed immature male rat.

LH and FSH release of immature male rats was remarkedably enhanced by LH-RH if primed with LH-RH one hour before. The effect of exogenous steroids on the action of the second LH-RH was investigated. C-18, C-19 and C-21 steroids in different doses were tested. Blood samples were collected from the jugular vein immediately before and 30 min after the second LH-RH injection. Serum LH and FSH were determined by respective radioimmunoassays. The concomitant increase of LH and FSH was not induced by all the steroids administered iv. Estrone or 17alpha-hydroxyprogesterone suppressed LH and FSH release. Estradiol-17beta preferentially suppressed LH release. Cortisone, progesterone or dehydroepiandrosterone significantly facilitated FSH release, whiel 20alpha-dihydroprogesterone or 20beta-dihydroprogesterone selectively promoted LH release. The sc injection of most steroids dissolved in oil tended to augment the acute release of LH but not FSH. 20alpha-Dihydroprogesterone was particularly potent in this concern. Dehydroepiandrosterone or androstenedione was effective in maintaining FSH release for a longer period. These data revealed that potentiated LH and FSH release induced by the second LH-RH was readily modified by steroids administered simultaneously.

Androgens↗

PubMed1982

Episodic luteinizing hormone (LH) secretion and the response of LH and follicle-stimulating hormone to LH-releasing hormone in aged men: evidence for coexistent primary testicular insufficiency and an impairment in gonadotropin secretion.

The influence of aging on episodic LH secretion and the release of LH and FSH after LRH administration was studied in 14 healthy men, aged 65-80 yr. Mean morning serum testosterone levels were reduced by 16% (P less than 0.05) and serum LH and FSH concentrations were increased by nearly 2- and 3-fold, respectively (P less than 0.01), compared to levels in young men. LH secretory episodes were evident and did not differ significantly in either amplitude or frequency from those of young men in spite of the higher mean LH concentrations. The increments in serum LH and FSH levels after LRH and the areas under the response curves were similar in aged and young men. However, the time of the peak LH response was significantly delayed with aging (P less than 0.001), suggesting an alteration in the control of the releasable LH pool. Further, LH levels were slower to fall after the peak in elderly men (P less than 0.01), suggesting prolonged secretion of hormone after LRH stimulation. These changes did not relate to the basal hypersecretion of LH in elderly men, as the responses in young men with primary gonadal failure did not differ from those in healthy young men (P = NS). The possibility that increased LH molecular size leads to its reduced clearance was not supported by the similar Sephadex G-100 elution profiles for LH in both basal and post-LRH sera from young and old men. Our data indicate that Leydig cell function is impaired in healthy elderly men as a result of primary testicular insufficiency. These studies further reveal the presence of an additional hypothalamic-pituitary disorder of gonadotropin secretion associated with the aging process.

Adult↗

PubMed1989

Effects of removal of carboxy-terminal extension from equine luteinizing hormone (LH) beta-subunit on LH and follicle-stimulating hormone receptor-binding activities and LH steroidogenic activity in rat testicular Leydig cells.

Residues 121-149 of equine LH beta (eLH beta) were removed by a simple mild acid treatment procedure. The modified eLH beta, des(121-149)eLH beta, was isolated by gel permeation chromatography on Sephacryl S-200. Recombination of des(121-149)eLH beta with eLH alpha and ovine LH alpha (oLH alpha) produced LH derivatives as efficiently as recombination with native eLH beta. In rat testicular LH radioligand assay systems employed in this study the potencies of the resulting LH preparations were, in order of decreasing potency: des(121-149)eLH beta:eLH alpha hybrid greater than eLH greater than eLH alpha + beta greater than oLH greater than des(121-149)eLH beta:oLH alpha greater than oLH alpha + eLH beta (1:0.82:0.67:0.15:0.02:0.006, eLH tracer; 1:0.88:0.67:0.21:0.02:0.006, hCG tracer). In a horse testicular LH radioligand assay with eLH tracer, only the equine LH derivatives were active, and the order of potencies was the same: des(121-149)eLH beta:eLH alpha hybrid greater than eLH greater than eLH alpha + beta (1:0.58:0.46). In a rat testicular Leydig cell steroidogenesis assay, eLH was the most active preparation, but the relative potencies of the other preparations remained unchanged: eLH greater than des(121-149)eLH beta:eLH alpha greater than eLH alpha + beta greater than oLH greater than des(121-149)eLH beta:oLH alpha greater than oLH alpha + eLH beta (1:0.61:0.55:0.27:0.004:0.003). We have previously reported that the hybrid consisting of native eLH beta and oLH alpha was inactive (less than 1%) in LH receptor and steroidogenesis assays. The data reported herein confirm this observation and demonstrate that the absence of LH activity in eLH beta:oLH alpha cannot be attributed to the C-terminal extension on eLH beta, since the des(121-149)eLH beta:oLH alpha hybrid LH is also inactive. Examination of the intrinsic FSH activity of eLH in both rat and chicken testicular FSH radioligand assays produced the following results; eLH, recombined eLH subunits, and des(121-149)eLH beta:eLH alpha were all of the same potency (13% and 0.9% as active as eFSH in rats and chickens, respectively). We conclude that the C-terminal extension on eLH and eCG beta-subunits is not involved in subunit association, LH receptor binding, or FSH receptor binding. The derivative des(121-149)eLH beta:eLH alpha provides a model compound that may be useful in determining the role, if any, of the glycoprotein hormone C-terminal extension that appears to have arisen independently at least twice in mammalian evolution.

Amino Acids↗

PubMed1978

Ultrastructure of rat pituitary LH gonadotrophs in relation to serum and pituitary LH levels following repeated LH-RH stimulation.

The effects of single and repeated LH-RH injections at 120 min intervals on female rat LH gonadotrophs and on pituitary and serum LH levels were investigated using electronmicroscopy and radioimmunoassay. A temporary stimulation of granule release, of protein and new granule synthesis and of the accumulation of lysosomal structures was found in LH cells after the first LH-RH injection. The temporary stimulations were massively enhanced after the second injection. These consecutive yet in their time-sequence overlapping processes account for the initial depletion of secretory granule content (3--15 min after LH-RH injection), for the subsequent regranulation and accumulation of granules above control levels (60--120 min after injection) and also for the reduction in the number of granules to control levels (150 min after LH-RH injection and thereafter). Increased polymorphic lysosomal structures are believed to be responsible for this reduction of excess granules. The amount of assayable pituitary and serum LH generally corresponds with the morphological changes observed in LH-gonadotrophs, thus further substantiating the above observations. A schema which summarizes the observed morphological and hormonal changes in their time-sequence in response to LH-RH stimulation depicts the short-term regulation of secretory processes in female gonadotrophs.

Animals↗