Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Luteinization”

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 199 records · Page 11Linked to original sources
PubMed1988

Mechanism controlling photostimulated luteinizing hormone secretion is different from preovulatory luteinizing hormone surge in Japanese quail (Coturnix coturnix japonica).

A so-called "night-interruption" experiment with a 15-min light pulse showed that a sensitive phase for the photoperiodic LH secretion in male Japanese quail extended over a period of 2 hr from 12.5 to 14.5 hr after dawn. Exposure of a 1-hr light pulse at this photosensitive phase to male quail kept under 8L:16D induced the increase of plasma LH concentrations just the same as quail transferred to 16L:8D. In the first few days of photostimulation either by night interruption or by long days, LH concentrations increased at several hours after the photosensitive phase and decreased to the basal levels before day-break. The amplitude and duration of this LH surge was somewhat like a preovulatory LH surge in females. However barbiturate anesthesia (pentobarbital and phenobarbital) administered on, before, or after the photosensitive phase did not block the LH increase by photostimulation. On the other hand, an injection of phenobarbital 14 hr before the expected ovulation blocked a preovulatory LH surge, even though the same drug failed to block photoinduced LH increase in females. These results indicate that the neuroendocrine mechanism involved in photostimulated LH release is different from that for an LH surge during an ovulatory cycle.

Animals↗
PubMed1995

Interaction between glutamate and luteinizing hormone-releasing hormone (LHRH) in lordosis behavior and luteinizing hormone release (LH): further studies on NMDA receptor mediation.

The present studies examine the effects of the glutamate agonist N-Methyl-D-Aspartic acid on lordosis responsiveness and LH release in estrogen-primed, ovariectomized rats. Groups of rats previously cannulated in the 3rd ventricle of the brain (IVT) were challenged with saline, NMDA and LHRH. A clear increase in lordosis-to-mount quotients (LQ) after IVT administration of 0.5, 0.75 and 1 microgram NMDA was found. LHRH (150 ng IVT) also enhanced LQ. High plasma LH levels were present in both cases. Intraventricular administration of the selective LHRH antagonist [D-p-Glu1, D-Phe2, D-Trp3,6]-LHRH (100 ng) was unable to prevent NMDA action on lordosis behavior. In contrast, it blunted LHRH enhancement of LQ. LH release evoked by either NMDA and LHRH was blocked by the LHRH antagonist. Present results support our previous view suggesting that glutamate, through NMDA receptors, participates in the regulation of lordosis behavior. Glutamate seems to exert its actions in the behavioral and endocrine patterns through different mechanisms; the first seems not to be mediated by LHRH, but the endocrine effect operates via LHRH release.

Animals↗
PubMedDate not supplied

Interactions between neuropeptide Y, luteinizing hormone-releasing hormone and estradiol in the control of luteinizing hormone release from cultured ovine pituitary cells.

This study used pituitary cells in culture firstly to test the hypothesis that NPY may augment the pituitary LH response to LHRH and secondly to determine whether this interaction is dependent on the presence of estradiol. LHRH (10(-10)-10(-6) M) caused a significant increase in LH secretion from dispersed ovine pituitary cells maintained in culture for six days, a response which was enhanced when cells were pretreated for three days with 4 x 10(-11) M estradiol. NPY 10(-10)-10(-6) M) had no effect on basal LH release from ovine pituitary cells maintained either in the presence or absence of estradiol. NPY (10(-10) and 10(-8) M) also had no effect on LHRH-stimulated LH release either in the presence or absence of estradiol. These results substantiate previous observations that physiologically relevant concentrations of estradiol enhance the LH response to LHRH in cultured ovine pituitary cells. However, in contrast to experiments carried out using rat pituitary cells in culture, the present data provide no evidence to support the hypothesis that NPY alone interacts with LHRH in the control of LH secretion from the ovine pituitary gland.

Animals↗
PubMed1975

Response of luteinizing hormone and follicle-stimulating hormone to different doses of synthetic luteinizing hormone-releasing hormone by intramuscular administration in normal and oligospermic men: preliminary report.

The response of LH and FSH levels to intramuscularly administered synthetic LH-RH was studied in two healthy volunteers and three oligospermic patients. Four tests with 50, 100, 250, and 500 mug of LH-RH, respectively, were carried out on each subject at 8 am; the interval between tests was one week. The serum levels of LH and FSH were determined by radioimmunoassay (double-antibody method) before each injection, and 60, 120, 180, and 240 minutes after each injection. No differences in the basal values of either hormone were observed. In both oligospermic and normal men, maximal responses were obtained with doses between 100 and 250 mug. With 500 mug, levels decreased rather than increased. Maximal peaks occurred between 60 and 180 minutes after injection. In the two normal subjects, the responses of LH and FSH were similar. Two of the three oligospermic patients showed discordant responses. From the results, we can assume that LH-RH doses between 100 and 250 mug should be used as a basis for chronic treatment.

Adult↗
PubMed1990

Detection of the ovulatory-luteinizing hormone surge with an enzyme-linked immunospecific human urinary luteinizing hormone assay: applicability to nonhuman primates.

Heterologous antibodies have frequently been used to develop assays in other species. Human urinary LH kits, widely available for predicting the LH surge, offer a unique opportunity to determine the timing of ovulation and mating in nonhuman primates. We tested three commercially available ovulation predictor kits for utility in two macaque species. Midfollicular, midcycle, and castrate urines and their corresponding serum samples were assessed for LH activity using established RIAs as well as urinary ovulation kits. Macaque LH did not sufficiently cross-react with the human urinary anti-LH antibodies in any of the predictor test kits. Although these kits offer excellent results in predicting ovulation by measurement of urinary LH in humans, they appear not to be applicable for urinary LH detection in rhesus nor cynomolgus macaques.

Animals↗
PubMed1998

Clinical pharmacology of recombinant human luteinizing hormone: Part I. Pharmacokinetics after intravenous administration to healthy female volunteers and comparison with urinary human luteinizing hormone.

OBJECTIVE: To assess the pharmacokinetics after i.v. administration of a recombinant human LH and to compare them to those of a reference hMG preparation containing urinary human LH. DESIGN: Prospective, dose-escalating, cross-over study. SETTING: Phase I clinical research environment. PATIENT(S): Twelve healthy pituitary down-regulated females. INTERVENTION(S): Subjects received single i.v. doses of 300, 10,000, and 40,000 IU of recombinant human LH, followed by a single i.v. dose of 300 IU of hMG, all separated by 1 week. MAIN OUTCOME MEASURE(S): Pharmacokinetic parameters. RESULTS: For both preparations, LH serum levels were well described by similar biexponential models. The pharmacokinetics of recombinant human LH were linear over the 300 to 40,000 IU range. After a rapid distribution phase with an initial half-life of 1 hour, both recombinant human LH and urinary human LH were eliminated with a terminal half-life of 10-12 hours. Total serum clearance was 1.7 L/h with < 4% and 30% of the dose being eliminated in the urine for recombinant human LH and urinary human LH, respectively. The volume of distribution at steady-state was approximately 10 L. Irrespective of the dose, recombinant human LH was well tolerated. CONCLUSION(S): The pharmacokinetics of recombinant human LH are linear with dose and similar to those of urinary human LH.

Adult↗
PubMed1998

Clinical pharmacology of recombinant human luteinizing hormone: Part II. Bioavailability of recombinant human luteinizing hormone assessed with an immunoassay and an in vitro bioassay.

OBJECTIVE: To assess the single-dose pharmacokinetics of a recombinant human LH preparation administered by the i.v., i.m., and s.c. route. DESIGN: Prospective, randomized cross-over study. SETTING: Phase I clinical research environment. PATIENT(S): Twelve healthy pituitary down-regulated females. INTERVENTION(S): Subjects received single i.v., i.m., and s.c. doses of 10,000 IU of recombinant human LH, each separated by 1 week. MAIN OUTCOME MEASURE(S): Pharmacokinetic parameters. RESULT(S): After single i.v. administration, the pharmacokinetics were described by a two-compartment model, after i.m. or s.c. administration, by a one-compartment model with zero order absorption and a lag time. Using the immunoassay, after i.v. administration initial half-life was 1 hour and terminal half-life was 10 hours (half-life was prolonged after extravascular administration, suggesting rate-limiting absorption). Total serum clearance was 2.6 L/h, and steady, state volume of distribution was 14 L. Observed Cmax, after i.m. and s.c. administration, was 43 IU/L with median tmax of 9 hours (i.m.) and 5 hours (s.c.). Bioavailability was 0.54 (i.m.) and 0.56 (s.c.). The pharmacokinetics of LH are comparable using an in vitro bioassay. CONCLUSION(S): The terminal half-life of recombinant human LH is around 12 hours and is slightly prolonged after extravascular administration. The pharmacokinetics are similar after i.m. and s.c. injection, and one-half the administered dose is available systemically.

Adult↗