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PubMed1992

Bovine luteinizing hormone (LH) isoforms and amounts of messenger ribonucleic acid for alpha- and LH beta-subunits in pituitaries of cows immunized against LH-releasing hormone.

Ovariectomized beef cows were actively immunized against LHRH to test the hypothesis that decreased stimulation of gonadotropes would alter the distribution of LH isoforms and amounts of mRNA for subunits of LH in the pituitary. Eight long-term (3 yr) ovariectomized beef cows were randomly assigned to one of two treatments: immunization against LHRH conjugated to human serum globulin (n = 4) and nonimmunization (control, n = 4). Mean concentration of serum LH in cows immunized against LHRH (1.0 +/- .83 ng/ml) was less (p = 0.01) than in control cows (5.0 +/- 0.83 ng/ml). Amounts of alpha- (p = 0.13) and LH beta-subunit (p = 0.10) mRNA tended to be reduced in cows immunized against LHRH compared to control cows. However, weight of the anterior pituitary and concentrations of LH in this gland did not differ (p = 0.90) among cows from the two groups. Pituitary extracts were chromatofocused on pH 10.5-7.0 gradients, and concentrations of LH in eluent fractions were determined by RIA. Extracts of all pituitaries resolved into nine isoforms (designated A through H and Z beginning with the most basic form). Only isoform F (mid-alkaline elution, pH = 8.8) was influenced by treatment (p = 0.05). Cows immunized against LHRH had a greater relative amount of isoform F (42.1 +/- 1.4%) than controls (37.2 +/- 1.4%). In summary, immunization of cows against LHRH altered 1) circulating concentrations of LH, 2) amounts of mRNA for the subunits of LH, and 3) distribution of intrapituitary LH isoforms without changing the concentrations of LH in the anterior pituitary.

Animals↗
PubMed1996

Direct actions of the luteinizing hormone-releasing hormone agonist, deslorelin, on anterior pituitary contents of luteinizing hormone (LH) and follicle-stimulating hormone (FSH), LH and FSH subunit messenger ribonucleic acid, and plasma concentrations of LH and FSH in castrated male cattle.

The objective in this study was to characterize direct effects of the LHRH agonist, deslorelin, on anterior pituitary gland function in male cattle in the absence of gonadal feedback. Castrated bulls (steers), 30 mo old, were allocated to four groups: group 1, control, no treatment (n = 8); group 2, five deslorelin implants (approximately 250 micrograms total deslorelin/day) for 42 days (n = 8); group 3, control+ LHRH (50 micrograms i.m.) at weekly intervals (n = 3); group 4, five deslorelin implants+LHRH as for group 3 (n = 3). Plasma LH was similar (p > 0.05) for steers in groups 1 and 2 on Day 0 and lower (p < 0.05) for steers in group 2 on Day 4, and continued to decrease to Day 41 (group 1, 1.71 +/- 0.20 ng/ml [mean +/- SEM]; group 2, 0.38 +/- 0.03 ng/ml [p < 0.001]). Mean plasma concentrations of FSH were similar (p > 0.05) for steers in groups 1 and 2 on Day 0 and lower (p < 0.05) for steers in group 2 on Day 7, and declined to Day 41 (group 1, 43.5 +/- 3.9 ng/ml; group 2, 17.5 +/- 1.5 ng/ml [p < 0.001]). Steers in group 3 showed increases in plasma LH after injection of LHRH on all occasions, while steers in group 4 did not show increases in plasma LH from Day 14 onward. Mean relative pituitary contents (arbitrary units) of LH beta- and FSH beta-subunit mRNAs were reduced on Day 42 in steers treated with deslorelin (LH beta: groups 1 and 3, 1.56 +/- 0.27; groups 2 and 4, 0.08 +/- 0.01 [p < 0.001]; FSH beta: groups 1 and 3, 1.01 +/- 0.08; groups 2 and 4, 0.34 +/- 0.07 [p < 0.001]). However, alpha-subunit mRNA was similar for control steers and steers treated with deslorelin (groups 1 and 3, 1.00 +/- 0.11; groups 2 and 4, 0.86 +/- 0.12 [p > 0.1]). Pituitary content of LH, but not FSH, was reduced in steers treated with deslorelin. In summary, steers treated with deslorelin showed desensitization to natural LHRH, and this was associated with reduced pituitary contents of LH and FSH beta-subunit mRNAs, a reduction in pituitary content of LH, and decreases in plasma concentrations of LH and FSH. This demonstrated, for the first time, a direct action of LHRH agonist on LH and FSH beta-subunit gene expression in cattle, independent of gonadal feedback. Also, there was a differential effect of treatment with deslorelin on gonadotropin alpha- and beta-subunit mRNA contents in the anterior pituitary.

Animals↗
PubMed1977

The relation between the age of the corpus luteum (CL) and the luteolytic effect of an LH-antiserum (LH-AS): comparison of hysterectomized pseudopregnant rats with intact pregnant rats for their response to LH-AS treatment at four stages of CL activity.

At one of four stages during the period of corpus luteum (CL) activity (day 9, day 12, day 15, or day 18) groups of hysterectomized pseudopregnant (PSP) rats and of intact pregnant (PRG) rats were compared for the effect of a single sc injection of an antiserum to LH (LH-AS) on progesterone secretion. Groups of control rats were injected sc with normal horse serum (NHS) at these same stages, and in all rats, the progesterone level in jugular blood serum was measured by RIA on the day of treatment and 24 and 72 h after treatment. Among the PRG rats, the controls' progesterone levels rose to a peak on day 15, and then slowly declined. LH-AS on day 9 induced abortion and a rapid, drastic and permanent fall in the progesterone level in all rats. On day 12, it induced a similar fall in progesterone, and abortion, in 4 of 10 rats; in the 6 which remained pregnant, a much less severe fall occurred 24 h after treatment, and by 72 h the level had returned to close to the initial one. On days 15 or 18, LH-AS induced neither abortion nor a significant change in the progesterone level from that seen in the controls. Among the PSP rats, the controls' progesterone levels tended to fall progressively after day 9; the average length of diestrus was about 21 days. At each of the four stages the LH-AS induced a rapid, drastic and permanent fall in the progesterone level. Early termination of the diestrus was easily discernible in the groups injected on days 9 or 12, but was obscured in the other groups because of the similarity in length of the expected remaining diestrus and the duration of the neutralizing effect of the LH-AS on LH in the circulation. The PSP rats' CL, thus, once they become dependent on LH (about day 9), remain so to the end of PSP. The PRG rats' CL seem to lose this dependency after day 12, but the possibility could not be eliminated that the dependency may shift from LH to a placental LH-like hormone.

Abortion, Induced↗
PubMed1976

Comparison of the anti-LH/FSH-RH and anti-ovulatory activities of (D-Phe2, D-Leu6)-LH-RH and (D-Phe2, D-Ala6)-LH-RH.

The anti-LH/FSH-RH and antiovulatory activities of [D-Phe2, D-Leu6]-LH-RH and [D-Phe2, D-Ala6]-LH-RH were compared in rats. Both peptides inhibited the LH and FSH release induced by LH-RH in immature male rats, but, 4 hr after the injection, [D-Phe2, D-Leu6]-LH-RH still suppressed the LH and FSH release whereas the [D-Phe2, D-Ala6]-LH-RH did not. When the peptides were administered in equal doses on the afternoon of the day of proestrus in 4-day cycling rats, [D-Phe2, D-Leu6]-LH-RH more completely inhibited the ovulation occurring on the following morning than [D-Phe2, D-Ala6]-LH-RH. Thus, the incorporation of D-Leucine into position six of the decapeptide chain gives a more potent inhibitor than that resulting from the insertion of D-Alanine.

Alanine↗
PubMedDate not supplied

Dose response inhibition of the circhoral pulsatile secretion of LH and FSH in rhesus monkeys by the administration of a potent inhibitory analogue of LH-RH ( [N-Ac-D-Trp1, 3, D-p-Cl-Phe2, D-Phe6, D-Ala10]-LH-RH).

The pulsatility of luteinizing hormone (LH) and follicle stimulating hormone (FSH) secretion was evaluated in chronically ovariectomized rhesus monkeys before and after the administration of [N-Ac-D-Trp1, 3, D-p-Cl-Phe2, D-Phe6, D-Ala10]-LH-RH) (IA-LHRH). Animals were divided into three groups (n = 4, each group) receiving, s.c.: 1) vehicle only (controls); 2) 0.5 mg IA-LH-RH; and 3) 2 mg IA-LH-RH. Twelve hours following drug administration, animals were chair-restrained and blood samples drawn every 10 minutes over a period of 4 hours via indwelling femoral vein catheters. LH and FSH levels were measured by RIA to determine the frequency, amplitude and increment of the pulses. Twelve hours after the administration of 0.5 mg or 2.0 mg of IA-LH-RH, levels of LH were reduced by 30 per cent and 68 per cent (P less than 0.001) and those of FSH by 34 per cent and 53 per cent (P less than 0.001 and P less than 0.002), respectively. Doses of 0.5 mg IA-LH-RH decreased the amplitude (20 per cent; P less than 0.001), increment (17 ng/ml; P less than 0.001) and frequency (2 per 4 h; P less than 0.001) of LH pulses. Administration of 2 mg IA-LH-RH produced a fall of increment (8 ng/ml; P less than 0.001), frequency (1 per 4 h; P less than 0.001) and pulse amplitude (26 per cent; P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Temporal relationship of the prolactin-dependent LH-induced LH receptor to the LH stimulus.

The time course for LH induction of luteinizing hormone (LH) receptors as reflected in binding of 125I-labeled hCG was investigated in hypophysectomized adult male rats. A low dose of oLH (10 micrograms) was administered to hypophysectomized adult male rats following pretreatments with prolactin, follicle-stimulating hormone (FSH), growth hormone (GH), or saline. Testicular binding of hCG was determined at different times following the LH injection using Leydig cell membrane preparations from a testicular homogenate. Seven days after hypophysectomy, hCG binding was at a nadir of 19 +/- 7% (mean +/- SD) of control values. Pretreatment with prolactin (100 micrograms/day) for 7 days was associated with a nonsignificantly different hCG binding that was 30 +/- 5% of control values. Prolactin pretreatment plus a single 10 micrograms LH i.p. injection increased 125I hCG binding up to 56 +/- 10% of control values within 30 minutes of the LH injection. Luteinizing hormone-induced hCG binding persisted at a high level (51 +/- 4% of control values) for 2 hours but returned to hypophysectomized control levels 6 hours after the i.p. LH injection. Seven days pretreatment with FSH or GH at 100 micrograms/day plus 10-micrograms LH injections was also tested. Neither FSH nor GH had a statistically significant effect on hCG binding nor could they mimic the ability of prolactin to allow for LH induction of hCG binding in the hypophysectomized adult male rats. These studies suggest that the induction or "up-regulation" of Leydig cell hCG binding by ovine LH is rapid and specifically dependent upon pre-exposure to prolactin.

Animals↗
PubMed1984

A comparison of the luteinizing hormone-releasing activities of synthetic chicken luteinizing hormone-releasing hormone (LH-RH), synthetic porcine LH-RH, and buserelin, an LH-RH analogue, in the domestic fowl.

The luteinizing hormone-releasing activities of synthetic chicken luteinizing hormone-releasing hormone (chLH-RH), synthetic porcine LH-RH (pLH-RH), and an analogue of LH-RH (buserelin, D-Ser-(But)6-des-Gly10-LH-RH ethylamide) were compared in the domestic fowl. In adult cockerels, intravenous injections of 0.5 or 1 microgram chLH-RH/kg released the same amount of LH as the same doses of pLH-RH; subcutaneous injections of 0.5 or 1 microgram buserelin/kg were about twice as effective as the same doses of pLH-RH. In laying hens, injections of 1, 10, 20, and 50 micrograms buserelin induced more sustained releases of LH than the corresponding doses of pLH-RH. Daily injections of 1 or 10 micrograms buserelin/bird or of 10 micrograms pLH-RH/bird for 12 days synchronized the timing of most ovipositions showing that the injections of releasing hormone could induce preovulatory surges of LH. In contrast with mammals, daily injections of buserelin in laying hens did not reduce pituitary responsiveness to the analogue. It is concluded that the structural difference between mammalian and chicken LH-RH does not affect their LH-releasing activities in the domestic fowl. Although the LH-releasing activity of buserelin in the hen is greater than that of pLH-RH, the difference in activity is not as great as that observed in most mammals. This view is strengthened by the finding that chronic treatment with buserelin, which exerts an antagonistic effect on ovulation in mammals, does not do so in the domestic hen.

Animals↗
PubMed1992

Neuropeptide Y potentiates luteinizing hormone (LH)-releasing hormone-induced LH secretion only under conditions leading to preovulatory LH surges.

We recently demonstrated that neuropeptide Y (NPY) potentiates the ability of pulsatile LHRH infusions to restore LH surges in pentobarbital (PB)-blocked, proestrous rats. In the present study we determined if specific endocrine conditions are necessary for the expression of these direct pituitary effects of NPY. Facilitatory actions of NPY were examined in the absence of gonadal feedback [ovariectomy (OVX)], in the presence of negative gonadal feedback (metestrus), after estrogen priming of the pituitary gland [OVX plus 30 micrograms estradiol benzoate (EB) 2 days before experiments], and after treatments which evoke preovulatory-like LH surges (OVX plus EB and 5 mg progesterone or P the morning of experiments). Rats received jugular catheter implants the day before experiments. On the day of experiments, hourly blood samples were taken from 1100-2100 h. At 1330 h, rats received injections of PB to block endogenous LHRH release, or saline. Every 30 min from 1400-1800 h, PB-treated rats received iv pulses of LHRH (15 ng/pulse) or saline, along with concurrent pulses of NPY (1 or 5 micrograms/pulse) or saline. Plasma samples were analyzed by LH RIA. In all cases, pulsatile administration of 15 ng LHRH resulted in plasma LH levels that were significantly elevated above saline-treated, PB-blocked controls. Only in the case of EB+P-treated rats did coadministration of 5 micrograms NPY along with LHRH significantly enhance LHRH-stimulated LH secretion (P < 0.001). NPY had no effect on LHRH-stimulated LH secretion in OVX, OVX + EB-treated, or metestrous rats. Pulsatile administration of either dose of NPY alone did not stimulate LH release in any of the four groups examined. These results demonstrate that the facilitatory effects of NPY on LHRH-stimulated LH secretion can be manifest only under the endocrine conditions required to produce full, preovulatory-like LH surges, i.e. after estrogen and P treatment.

Animals↗
PubMed1976

Secretion rates of LH and FSH during infusion of LH-FSH/RH in normal women and in patients with secondary amenorrhea: suggestive evidence for two pools of LH and FSH.

Normal women in the early follicular phase and in the luteal phase of the cycle, and patients with secondary amenorrhea received on consecutive days a rapid intravenous injection (50 mug) and a two or four-hour infusion (25 mug/h) of synthetic LH-FSH/RH. The responses of LH and FSH were evaluated by the measured plasma concentrations, as well as by the calculated pituitary secretion rates and by the amounts of hormone released. To estimate these pituitary secretion rates of LH and FSH, a simplified mathematical model is proposed. During an infusion of LH-FSH/RH the secretion rates of both LH and FSH increased in the three groups of women in a biphasic way with a dip after 1 to 2h of infusion, suggesting that besides the pool mobilized by a rapid intravenous injection of LH-FSH/RH there is a second pool of (stored) gonadotropins. For LH the increase above baseline concentrations was higher in group II (luteal phase) than in group I (follicular phase) or in group III (amenorrhea) and this both after a bolus injection and during infusion of LH-FSH/RH. For FSH a similar pattern of response prevailed during an infusion of LH-FSH/RH. After a bolus administration, however, the FSH release was relatively higher in group III (amenorrhea) than in both groups of normal women in which the increases were about the same. The latter finding suggests that the first pool of FSH is released by a different mechanism than the second pool.

Adult↗
PubMed1977

Serum LH, FSH and testosterone response to the administration of a new LH-RH analog, D-Trp6-LH-RH, in normal men.

A long-acting superactive analog of LH-RH, D-Trp6-LH-RH was given to 23 normal men by several routes of administration (iv, im, sc, continuous infusion) and in increasing doses of 1 to 50 microgram. LH and FSH responses were obtained at doses as low as 2.5 microgram. The maximal absolute LH and FSH increment in response to a 10 microgram iv bolus injection of this analog was similar to 100 microgram of LH-RH. In addition, after administration of the analog the LH and FSH level was maintained at a higher than basal level for at least 8 hours. With a 50 microgram iv bolus injection, from 30 minutes onwards the increases in LH levels were significantly greater (P less than 0.05) than those elicited by the 10 microgram dose for at least 8 hours. Maximum release of LH and RSH was observed when this same dose was given as continuous infusion for 8 hours (P less than 0.05). There seemed to be no significant differences between the im and sc routes. Following the administration of the D-Trp6-LH-RH, testosterone levels were maintained above the normal values (P less than 0.02). The high potency and prolonged duration of action of this compound suggest its potential usefulness for increasing testosterone levels and for stimulation of spermatogenesis in men.

Follicle Stimulating Hormone↗
PubMed1980

[Increased and prolonged release of lh and fsh on intravenous administration of a synthetic analogue of lh-rh [d-ser(tbu)6-ea10-lh-rh] in healthy men of various age groups (author's transl)].

Healthy male subjects of various age groups respond to the administration of D-Ser(TBU)6-EA10-LH-RH, an analogue of LH-RH substituted in positions 6 and 10, by a prolonged and increased release of LH and FSH. Increased serum concentrations of LH and FSH were observed 20 minutes after intravenous administration of the compound. Maximum concentrations of LH and FSH were seen after 60, and 60 to 240 minutes, respectively. Serum concentrations of both gonadotropins remained elevanted for up to 8 hours after the administration of 10 microgram of the LH-RH analogue. A dose response relationship was observed with regard to the serum concentrations of LH and FSH over the range of 1.25 to 5.0 microgram of the LH-RH analogue. The administration of 10 or 20 microgram of the compound, however, did not cause a further rise in plasma FSH, although the release of LH was further enhanced.

Adolescent↗
PubMed1987

[Salivary LH as an ovulation indicator: comparison between salivary LH, serum LH and ultrasonic findings].

A radioimmunological method of salivary LH determination has been developed as a new non invasive approach to hormonal ovulation detection. In this study salivary LH patterns have been compared to serum LH peak and daily sonographic assessment of follicle maturation in 15 spontaneous cycles of 9 women experienced in self-observation of their cycles (NFP). The day where the mature follicle was no longer visible sonographically was labelled day 0. Serum LH peaks occurred in 11 out of 15 cycles on day -1, two times on days -2 and 0 and preceded salivary LH peaks in 8 out of 15 cycles. The latter coincided in 7 cycles with day 0 in two cycles each with days -1 and +1 and in 4 cycles with day -2. Thus 13/15 serum- and 11/15 salivary-LH peaks occurred within +/- one day of the disappearance of the mature follicle. A time lag of up to six hours between the sampling of saliva and serum might explain the difference in the respective peak days, however, more studies into the kinetics of LH transport and its circadian rhythmicity seem necessary. Nevertheless, in principle also the salivary LH peak is considered a suitable indicator of ovulation.

Adult↗
PubMed1982

Pulsatile luteinizing hormone (LH) patterns in ovariectomized rats: involvement of norepinephrine and dopamine in the release of LH-releasing hormone and LH.

Cannulated ovariectomized (OVX) rats were bled every 10 min for 2 h to characterize their individual patterns of LH release. After the last sample, all rats were decapitated, and their brains were removed for analysis of LHRH, norepinephrine (NE), and dopamine (DA) levels in median eminence (ME), arcuate-ventromedial, and suprachiasmatic-medial preoptic region (Sch-PO) to determine if changes in NE, DA, and LHRH levels in any of those areas could be observed at different points during the pulsatile release of LH. The results showed that when LH levels started to increase, NE levels peaked in the Sch-PO, whereas a sharp drop in DA and LHRH levels in the ME was detected, which may reflect an acute release in the ME of both DA and LHRH. When LH levels reached peak values, NE levels in the Sch-PO returned to lower values, and DA and LHRH in the ME rose to higher levels. Inhibition of NE synthesis with diethyldithiocarbamate resulted in the suppression of LH pulses. L-Dopa administered after diethyldithiocarbamate induced an increased release of LH in both OVX and OVX, estrogen-primed rats with a simultaneous inhibition of PRL release. Peak levels of LH after L-dopa treatment coincided with increased DA levels in the ME, no change in NE, and a clear drop in LHRH. The results suggest that both NE and DA are involved in the pulsatile release of LH in OVX rats.

Animals↗
PubMed1994

Cumulus and oocyte maturation and in vitro and in vivo fertilization of oocytes 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.

Crossbred heifers (n = 103) were synchronized to estrus with prostaglandin (PGF2 alpha) and superovulated with follicle stimulating hormone (FSH-P). Animals were ovariectomized every 12 hr after the PGF2 alpha injection (n = 7 to 9/time) up to 108 hr to monitor the follicular, hormonal, and oocyte changes associated with follicular development and ovulation. Twenty-eight animals were implanted with Norgestomet implants 12 hr before PGF2 alpha and ovariectomized at 72, 84, 96, and 108 hr post PGF2 alpha injection to monitor effects of progesterone and suppression of the luteinizing hormone (LH) surge on oocyte maturation and quality. Follicular fluid was collected and analyzed for progesterone, estradiol, prolactin, and glycosaminoglycan content in conjunction with cumulus maturation and nuclear stage of oocyte maturation. Analysis of in vivo matured oocytes by in vitro fertilization was carried out at 60, 72, 84, and 96 hr post PGF2 alpha and in vitro matured oocytes at 12 to 108 hr post PGF2 alpha. No developmental changes in cumulus cells surrounding the oocyte of small follicles was noted (< or = 4 mm dia) indicating a static population. Medium (> 4 < or = 8 mm) and large size (> 8 mm) follicles developed to the corona radiata and loose cumulus stages in animals in which an LH surge was detected but cumulus status remained primarily in the tight cumulus stage for animals without an LH surge. The estradiol-to-progesterone ratio for tight cumulus (TC), corona radiata (CR), and loose cumulus (LC) stages was 1.8 +/- .1, 1.0 +/- .1, and .4 +/- .2, respectively (P < .01). Nuclear maturation of oocytes in small follicles from animals without a detectable LH surge seem to indicate early maturation (48 to 72 hr post PGF2 alpha) in conjunction with a high percent of degenerate oocytes not seen in animals exhibiting an LH surge. Oocytes from medium size follicles matured to germinal vesicle breakdown (GVBD) and early meiosis (metaphase I; MI) stages of development in all treatments. Most oocytes were degenerate in Norgestomet-implanted animals. Oocytes from large follicles (> 8 mm dia) from animals exhibiting an LH surge were in MI and metaphase II (MII) stages (48 to 84 hr post PGF2 alpha) in preparation of ovulation whereas oocytes from animals not exhibiting an LH surge had oocytes that early matured to MII (48 to 72 hr post PGF2 alpha), later regressing to degenerate oocytes (84 to 108 hr). Follicular progesterone, estradiol, and prolactin increased with oocyte maturation, particularly in medium and large follicles.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1996

Characteristics of luteinizing hormone (LH) and testosterone secretion, pituitary responses to LH-releasing hormone (LHRH), and reproductive function in young bulls receiving the LHRH agonist deslorelin: effect of castration on LH responses to LHRH.

Young bulls were treated with graded dosages of the LHRH agonist deslorelin to ascertain 1) whether increased testosterone secretion persisted over a wide dose range of agonist; 2) whether elevated testosterone was maintained long-term and, if so, what effects there were on reproductive function; and 3) what pituitary responses to exogenous LHRH occurred in intact and castrated bulls receiving deslorelin. In three experiments, bulls received dosages of agonist ranging from approximately 0.15 to 29.0 micrograms deslorelin/kg live weight/day, by means of either bioimplants or injections. At all dosages, deslorelin induced an acute increase in plasma LH concentrations that declined after 24 h but remained at greater concentrations than in controls, although the differences were relatively small. Profiles of LH in bulls treated with deslorelin were characterized by tonic secretion with no clear evidence of LH pulses. Plasma testosterone concentrations were increased at all dosages of deslorelin and in one experiment remained greater than in controls for over 100 days of treatment. This increase was associated with an increase in the rate of testis growth; however, there were no apparent improvements in semen parameters. Bulls receiving deslorelin did not show a typical postcastration rise in plasma LH concentrations, and neither intact nor castrated bulls receiving deslorelin showed an increase in plasma LH after injection of natural sequence LHRH. The absence of endogenous LH pulses and lack of response to exogenous LHRH suggested that the anterior pituitary in bulls receiving LHRH agonist becomes desensitized. However, LH secretion persisted in a tonic manner and was associated with elevated plasma testosterone concentrations. The failure of both intact and castrated bulls receiving deslorelin to respond to exogenous LHRH suggested direct effects of deslorelin on the pituitary, rather than an interaction with steroid feedback.

Animals↗
PubMed1975

Daytime titers of testosterone, LH, estrone, estradiol, and testosterone-binding protein: acute effects of LH and LH-releasing hormone in men.

Four normal 18-20 yr-old men were studied on 3 occasions, from 0830 h to 1500 h. The baseline for each study consisted of 3 or 4 measurements of the respective hormone obtained between 0830 and 0900 h. In the control studies mean testosterone (T) fell by 43% (P less than 0.01) during the final 30 min. The fall was gradual throughout the day and was significant by 1100 h (P less than 0.05). Administration of LH and LH-releasing hormone (LHRH) at 0900 h resulted in 9-fold (5 min) and 3-fold (30 min) higher concentrations of LH respectively. LH declined more slowly after LHRH. Titers of T rose to the 0830-0900 h mean 130 min after LH but were never significantly elevated; the occurrence of a significant drop in mean T was delayed for 70 min. After LHRH there was a nonsignificant 24% increase of the mean T followed by a slow decline; however, T did not fall significantly below the mean baseline level. In contrast, in 2 of the 4 subjects LHRH resulted in rises in T levels (P less than 0.05) above the basal titers. Testosterone-binding globulin (TeBG) mean titers showed no diurnal rhythm in the control studies. There were statistically significant elevations of mean TeBG 150 min after LH and 340 to 370 min after LHRH, as well as sustained increases during the final 30 to 210 min of 1 or 2 individuals in each group. The reason for these increases in TeBG is not presently known. Estrogen analyses performed in all studies on 2 of the subjects revealed: 1) afternoon titers of estrone were lower than baseline in all 6 studies, 2) there was no diurnal rhythm for estradiol in control studies, and 3) estradiol increased during the final 2.5 to 3 h after LHRH (P less than 0.01), but after LH it was not altered in 1 man and was lower in the other.

Adolescent↗
PubMed1997

Expression of horse and donkey LH in COS-7 cells: evidence for low FSH activity in donkey LH compared with horse LH.

Horse (Equus caballus) luteinizing hormone (eLH) and chorionic gonadotrophin (eCG), which have the same amino acid sequence, are unusual in that, although they express only LH activity in equids, they express dual LH and FSH activities in all other species tested. Donkey (Equus asinus) LH (dkLH) and CG (dkCG), which also share an identical peptide backbone, have been less well characterized and conflicting results concerning their FSH activity in heterologous species have appeared in the literature. In order to assess and compare the intrinsic LH and FSH activities of the horse and donkey LHs in heterologous species, recombinant eLH (r.eLH/CG) and recombinant dkLH (r.dkLH/CG) were expressed, for the first time, in COS-7 cells. Their LH activities were assessed in a rat Leydig cell bioassay, and their FSH activities were estimated in a bioassay using Y1 cells stably expressing the human FSH receptor. Human CG (hCG) was expressed (r.hCG) and analysed in the same system. The results showed that, whereas r.dkLH/CG was about twice as active as r.eLH/CG in the LH bioassay, it was five times less active than r.eLH/CG in the FSH bioassay; r.hCG was about three times less active than r.eLH/CG in the LH bioassay but was completely inactive in the FSH bioassay. These results confirm that dkLH/CG possesses significant FSH activity in heterologous species that is not attributable to contamination with FSH.

Animals↗
PubMed1984

Luteinizing hormone (LH) receptor aggregation: modification of ferritin-LH binding and aggregation by prostaglandin F2 alpha and ferritin-LH.

The interaction of LH and its receptor was investigated by ultrastructural analysis of ferritin-LH (FELH) binding to isolated rat luteal cells in the absence and presence of prostaglandin F2 alpha (PGF2 alpha), an inhibitor of LH-stimulated cAMP production. FELH, with a molar ratio of FE to LH of 1:1, bound specifically to LH receptors, either singly or in small groups (microaggregates), at intervals on luteal cell surfaces. FELH elicited a dose-dependent increase in progesterone production, and its binding increased with increased FELH concentration. The number of LH receptors per cell, estimated from particle counts, was about 6.2 +/- 0.6 X 10(4), similar to estimates from Scatchard analysis of [125I]iodo-hCG binding. Microaggregate size increased in parallel with FELH binding. Only partial aggregation was seen at concentrations of FELH that elicited near-maximal progesterone secretion. Aggregation continued to increase at FELH concentrations beyond that required to elicit maximal progesterone secretion. In the presence of PGF2 alpha, FELH-stimulated progesterone production was attenuated, and FELH binding decreased from 2.9 +/- 0.4 X 10(4) to 2.1 +/- 0.3 X 10(4) receptors/cell. PGF2 alpha did not alter microaggregate size on cells labeled with FELH at 4 C when membrane fluidity was already reduced, but did substantially reduce microaggregate size at 37 C. We conclude that FELH binds initially at random sites on membranes of isolated luteal cells and that as binding increases, receptors aggregate into small groups. Furthermore, microaggregates are related in part to receptor occupancy and possibly also to levels of cAMP or activation of the adenylate cyclase mechanism.

Animals↗