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Lutein ester in serum after lutein supplementation in human subjects.

Lutein, one of the major carotenoids present in serum, is also widely consumed by most populations. For the purpose of testing the potential health benefits of several carotenoids, lutein was supplied as part of an intervention trial to test whether the consumption of these food constituents reduces oxidative damage to human tissue components. Lutein from a natural source (15 mg/d as mixed ester forms) was supplied for 4 months to eighteen non-smoking, apparently healthy volunteers (nine men, nine women) aged 25-45 years. The serum carotenoid profile was analysed at baseline and monthly thereafter. On average, lutein concentrations increased 5-fold after the first month of supplementation (mean 1.34 (range 0.6-3.34) mumol/l). On reviewing the results, in those volunteers whose lutein levels surpassed 1.05 mumol/l (fourteen of seventeen), we tentatively identified lutein monopalmitate along with another unidentified ester (possibly from a monoketocarotenoid) in serum. Lutein levels returned to baseline values and ester forms were not present 3 months after supplementation was discontinued. Their concentrations did not correlate with, and represented less than 3% of, lutein levels achieved in serum. They were observed before development of, and despite the presence of, carotenodermia. To our knowledge, this is the first time xanthophyll esters have been described in human serum. In view of the fact that xanthophyll esters have not been previously reported in serum and chylomicrons, it seems unlikely that these ester forms would be a reflection of the contents of the capsule. They may indicate a 'ceiling effect' on or saturation of the transport capacity for xanthophylls, and may have been re-esterified in vivo because of the unusual dietary conditions. The determination of the physiological importance of this finding will require further investigation, although neither haematological nor biochemical changes were detected.

Adult↗

Premature luteinization is not eliminated by pituitary desensitization with leuprolide acetate in women undergoing gonadotrophin stimulation who demonstrated premature luteinization in a prior gonadotrophin-only cycle.

A total of 40 women who demonstrated premature luteinization (serum progesterone > or = 3.5 nmol/l (1.1 ng/ml) on or before the day of human chorionic gonadotrophin (HCG) administration) during ovarian stimulation with human menopausal gonadotrophins (HMG) were restimulated in 46 subsequent cycles after pituitary desensitization with the gonadotrophin-releasing hormone agonist (GnRHa, 1 mg), leuprolide acetate. Five women were treated with a double dose of agonist (2 mg) when premature luteinization was determined on the single dose protocol. In HMG-only cycles, a frank luteinizing hormone (LH) surge was detected in 30 cycles; 15 cycles were cancelled because of premature ovulation. In agonist cycles there were no cancellations, although 25 cycles demonstrated premature luteinization and in six cycles a frank LH surge was detected. Doubling the dose of the agonist did not prevent premature luteinization. Agonist cycles with and without premature luteinization did not differ in any in-vitro fertilization (IVF) outcome parameters (ampoules of gonadotrophins, day of HCG administration, peak oestradiol concentration, number of oocytes retrieved, fertilized, transferred or cryopreserved). We conclude that in patients who demonstrate premature luteinization in a gonadotrophin-only cycle, pituitary desensitization may not completely eliminate subtle luteinization or a frank LH surge.

Chorionic Gonadotropin↗

Differentiation between lutein monoester regioisomers and detection of lutein diesters from marigold flowers (Tagetes erecta L.) and several fruits by liquid chromatography-mass spectrometry.

Liquid chromatography-atmospheric pressure chemical ionization mass spectrometry (LC-APCIMS) was employed for the identification of eight lutein monoesters, formed by incomplete enzymatic saponification of lutein diesters of marigold (Tagetes erecta L.) by Candida rugosa lipase. Additionally, the main lutein diesters naturally occurring in marigold oleoresin were chromatographically separated and identified. The LC-MS method allows for characterization of lutein diesters occurring as minor components in several fruits; this was demonstrated by analysis of extracts of cape gooseberry (Physalis peruviana L.), kiwano (Cucumis metuliferus E. Mey. ex Naud.), and pumpkin (Cucurbita pepo L.). The assignment of the regioisomers of lutein monoesters is based on the characteristic fragmentation pattern: the most intense daughter ion generally results from the loss of the substituent (fatty acid or hydroxyl group) bound to the epsilon-ionone ring, yielding an allylic cation. The limit of detection was estimated at 0.5 microg/mL with lutein dimyristate as reference compound. This method provides a useful tool to obtain further insight into the biochemical reactions leading to lutein ester formation in plants.

Asteraceae↗

Slowly reversible de-epoxidation of lutein-epoxide in deep shade leaves of a tropical tree legume may 'lock-in' lutein-based photoprotection during acclimation to strong light.

The kinetics of response to strong light have been examined in deeply shaded leaves of the tropical tree legume (Inga sp.) which have extraordinarily high levels of the alpha-xanthophyll lutein-epoxide that are co-located in pigment-protein complexes of the photosynthetic apparatus with the beta-xanthophyll violaxanthin. As in other species, rapidly reversible photoprotection (measured as non-photochemical chlorophyll fluorescence quenching) is initiated within the time frame of sun-flecks (minutes), before detectable conversion of violaxanthin to antheraxanthin or zeaxanthin. Photoprotection is stabilized within hours of exposure to strong light by simultaneously engaging the reversible violaxanthin cycle and a slowly reversible conversion of lutein-epoxide to lutein. It is proposed that this lutein 'locks in' a primary mechanism of photoprotection during photoacclimation in this species, converting efficient light-harvesting antennae of the shade plant into potential excitation dissipating centres. It is hypothesized that lutein occupies sites L2 and V1 in light-harvesting chlorophyll protein complexes of photosystem II, facilitating enhanced photoprotection through the superior singlet and/or triplet chlorophyll quenching capacity of lutein.

Acclimatization↗

Dose-related inhibition of acute luteinizing hormone response during luteinizing hormone-releasing hormone agonist treatment for uterine leiomyoma.

Twenty-six women with uterine leiomyoma were treated for 6 months with subcutaneous injections of the luteinizing hormone-releasing hormone agonist buserelin. Eight women received 200 micrograms daily, eight women received 350 micrograms daily, and 10 women after initial administration of 200 micrograms every 8 hours for 7 days, 500 micrograms of buserelin was administered daily. After 1, 3, and 6 months of treatment, serum luteinizing hormone levels were measured before and 4 and 8 hours after the administration of buserelin. The area under the curve for acute luteinizing-hormone response was then individually calculated. The inhibition of acute luteinizing hormone response during luteinizing hormone-releasing hormone agonist treatment was proportional to the dosage used and remained constant during the treatment period.

Adult↗

Effect of preovulatory estradiol concentrations on luteinizing hormone diurnal secretory patterns: a hypothesis for the timing of the luteinizing hormone surge.

The effect of preovulatory estradiol concentrations on 24-hour patterns of luteinizing hormone secretion was studied in six women with normal menstrual cycles. Blood samples were collected every 15 minutes for 24 hours before and after 7 days of estradiol benzoate administration, which achieved mean (+/- SE) estradiol concentrations of 424 +/- 54 pg/ml. The luteinizing hormone pulse frequency decreased significantly during sleeping hours both before (p less than 0.05) and after (p less than 0.005) estradiol benzoate administration. After estradiol benzoate, there also was diurnal variation in overall mean luteinizing hormone concentrations, which markedly increased secretion in the morning hours. The diurnal changes in luteinizing hormone secretion varied inversely with those of prolactin. These findings are consonant with the observation that the onset of the preovulatory luteinizing hormone surge in women occurs most frequently in the early morning hours.

Adult↗

Prolonged inhibition of luteinizing hormone and testosterone levels in male rats with the luteinizing hormone-releasing hormone antagonist SB-75.

Inhibitory effects of the potent antagonist of luteinizing hormone-releasing hormone N-Ac-[3-(2-naphthyl)-D-alanine1,4-chloro-D-phenylalanine2,3- (3-pyridyl)-D- alanine3,D-citrulline6,D-alanine10]luteinizing hormone-releasing hormone (SB-75) free of edematogenic effects were investigated in male rats. In a study to determine the effect on luteinizing hormone levels in castrated male rats, SB-75 was injected s.c. in doses of 0.625, 1.25, 2.5, 5.0, and 10 micrograms. Blood samples were taken at different intervals for 48 hr. All doses of SB-75 significantly decreased luteinizing hormone levels for greater than 6 hr (P less than 0.01); this inhibition lasted for greater than 24 hr (P less than 0.01) with a dose of 5.0 micrograms and greater than 48 hr with 10 micrograms (P less than 0.05). Serum testosterone levels were also measured in intact male rats injected with SB-75 in doses of 25, 50, and 100 micrograms. All doses produced a dramatic fall in testosterone to castration levels 6 hr after injection (P less than 0.01); this inhibition of serum testosterone was maintained for greater than 72 hr, but only the 100-micrograms dose could keep testosterone in the castration range for greater than 24 hr (P less than 0.01). In another study using a specific RIA, we obtained the pharmacokinetic release pattern of SB-75 from two sustained delivery formulations of SB-75 pamoate microgranules and examined their effect on serum testosterone. After a single i.m. injection of 20 mg of one batch of microgranules, a large peak corresponding to SB-75 at 45.8 ng/ml was observed, corresponding to the "burst" effect. Levels of the analog decreased to 19.6 ng/ml on day 2, gradually reached a concentration of 4.7 ng/ml on day 7, and kept declining thereafter. Testosterone levels were reduced on day 1 (P less than 0.01) and were maintained at low values for greater than 7 days (P less than 0.05). In rats injected with 10 mg of SB-75 pamoate microgranules of the second batch, SB-75 serum levels rose to 33 ng/ml 3 hr after administration and then fell gradually to approximately 3.4 ng/ml on day 16, but a second small peak was seen on day 28. Subsequently, the analog levels decreased slowly to 2.9 ng/ml on day 42. At this time, testosterone serum levels were still significantly lower than in controls. These overall results demonstrate the efficacy of SB-75 in the suppression of the pituitary-gonadal axis. This modern luteinizing hormone-releasing hormone antagonist can possibly be used for treating sex hormone-sensitive cancers and other disorders.

Animals↗

Ovarian stromal tumors containing lutein or Leydig cells (luteinized thecomas and stromal Leydig cell tumors)--a clinicopathological analysis of fifty cases.

Fifty ovarian stromal tumors that had a predominant pattern of fibroma or thecoma but also contained cells typical of steroid hormone-secreting cells are reported. Forty-six tumors were classified as luteinized thecomas because the steroid cells resembled lutein cells and lacked crystalloids of Reinke. Four were classified as stromal Leydig cell tumors because crystalloids were identified in the steroid cells. The luteinized thecomas occurred at an average age of 46 years and were associated with estrogenic manifestations in 50% and androgenic changes in 11% of the cases. In the remaining cases there was no clinical or pathological evidence of steroid hormone production at the time of diagnosis. Six patients, two of whom were virilized, were pregnant. Four tumors appeared malignant on histologic examination. One of these tumors was rapidly fatal, the outcome is unknown in a second case, the third patient is alive and well at 5 years, and the fourth tumor was diagnosed too recently for evaluation of its behavior. The stromal Leydig cell tumors occurred at an average age of 61 years and were associated with virilization in one case, endometrial hyperplasia in another case, and endometrial hyperplasia with carcinoma in a third case. The fourth tumor was unassociated with endocrine manifestations. Luteinized thecomas and stromal Leydig cell tumors are indistinguishable except for the presence of crystalloids of Reinke in the latter. In view of the prolonged search that is necessary to find these structures in some stromal Leydig cell tumors and their well-known absence in the majority of testicular Leydig cell tumors, it is reasonable to assume that an unknown proportion of tumors in the luteinized thecoma category are unrecognized stromal Leydig cell tumors.

Adolescent↗

Expression of 11beta-hydroxysteroid dehydrogenase (11betaHSD) proteins in luteinizing human granulosa-lutein cells.

In a range of tIssues, cortisol is inter-converted with cortisone by 11beta-hydroxysteroid dehydrogenase (11betaHSD). To date, two isoforms of 11betaHSD have been cloned. Previous studies have shown that human granulosa cells express type 2 11betaHSD mRNA during the follicular phase of the ovarian cycle, switching to type 1 11betaHSD mRNA expression as luteinization occurs. However, it is not known whether protein expression, and 11betaHSD enzyme activities reflect this reported pattern of mRNA expression. Hence, the aims of the current study were to investigate the expression and activities of 11betaHSD proteins in luteinizing human granulosa-lutein (hGL) cells. Luteinizing hGL cells were cultured for up to 3 days with enzyme activities (11beta-dehydrogenase (11betaDH) and 11-ketosteroid reductase (11 KSR)) and protein expression (type 1 and type 2 11betaHSD) assessed on each day of culture. In Western blots, an immunopurified type 1 11betaHSD antibody recognized a band of 38 kDa in hGL cells and in human embryonic kidney (HEK) cells stably transfected with human type 1 11betaHSD. The type 2 11betaHSD antibody recognized a band of 48 kDa in HEK cells transfected with human type 2 11betaHSD cDNA but the type 2 protein was not expressed in hGL cells throughout the 3 days of culture. While the expression of type 1 11betaHSD protein increased progressively by 2.7-fold over 3 days as hGL cells luteinized, both 11betaDH and reductase activities declined (by 52.9% and 34.2%; P<0.05) over this same period. Changes in enzyme expression and activity were unaffected by the suppression of ovarian steroid synthesis.

11-beta-Hydroxysteroid Dehydrogenase Type 2↗

Titrating luteinizing hormone surge requirements for ovulatory changes in primate follicles. II. Progesterone receptor expression in luteinizing granulosa cells.

The events in granulosa cells that are initiated by the midcycle LH surge during luteinization of the primate follicle are poorly defined. This study was designed 1) to determine whether an ovulatory dose of hCG can induce progesterone receptors (PR) in macaque granulosa cells, and if so, 2) to begin titrating gonadotropin requirements for PR expression and progesterone production by luteinizing granulosa cells. Rhesus monkeys were treated with human FSH and LH for up to 9 days to stimulate the growth of multiple follicles. The next day, animals (n = 4-5/group) received: 1) no ovulatory stimulus; 2) 1000 IU hCG, im; 3) one injection of 100 micrograms GnRH, sc (GnRH-1); 4) three injections of GnRH (GnRH-3) at 3-h intervals (0800, 1100, and 1400 h); or 5) two injections of 50 micrograms GnRH agonist (GnRHa), sc, 8 h apart (0800 and 1700 h). Granulosa cells obtained by follicle aspiration 27 h after the hCG or initial GnRH/GnRHa injection or on days 8 or 10 from animals receiving no ovulatory stimulus were processed for indirect immunocytochemistry using a monoclonal antibody to human PR (JZB39). Specific staining for PR, determined by comparing cells incubated with PR antibody vs. a nonspecific antibody, was undetectable in granulosa cells from monkeys without an ovulatory stimulus. In contrast, the majority (64 +/- 5%) of cells from hCG-treated animals stained intensely for PR. In the GnRH/GnRHa groups, granulosa cells from only one animal (i.e. one GnRH-3 monkey) showed positive staining for PR. During 24-h culture in Ham's F-10 medium containing 10% monkey serum, basal progesterone production by cells from the hCG-treated group (2163 nmol/L.8 x 10(4) cells) was higher than that by cells from the no ovulatory stimulus/GnRH-1/GnRH-3/GnRHa groups (60, 111, 194, and 332 nmol/L, respectively). However, granulosa cells from the hCG-treated group were less responsive to hCG in vitro in terms of enhanced progesterone production (2 times control levels) than cells from the other four groups (up to 30 times control levels). This study provides direct evidence that an ovulatory dose of hCG induces PR expression in granulosa cells of luteinizing follicles during stimulated cycles in rhesus monkeys. However, repeated injections of GnRH/GnRHa that produced surge levels (greater than 100 ng/mL) of endogenous LH for up to 14 h failed to induce PR expression or progesterone production by granulosa cells. Thus, an extended LH surge more typical of that in the normal menstrual cycle (48-50 h) may be necessary for PR expression and luteinization of granulosa cells in primate follicles.

Animals↗

Absence of an effect of naloxone, an opioid antagonist, on luteinizing hormone release in vivo and luteinizing hormone-releasing hormone I release in vitro in intact, castrated, and food restricted cockerels.

The possibility that the tonic secretion of luteinizing hormone (LH) and chicken luteinizing hormone-releasing hormone I (LHRH-I) is regulated by an inhibitory action of endogenous opioid peptides was investigated in cockerels using the opiate receptor antagonist, naloxone. Baseline concentrations of plasma LH in the experimental cockerels were increased by surgical castration or reduced by limiting food intake. Baseline and K(+)-induced releases of LHRH-I from perifused mediobasal-preoptic hypothalami from castrated cockerels were higher than those from hypothalami from intact cockerels. Similarly, baseline and K(+)-induced releases of LHRH-I from perifused mediobasal hypothalami from fully fed cockerels were higher than those from the hypothalami from fasting cockerels. Intravenous injections of 0.1, 1, or 10 mg naloxone/kg body weight failed to increase the concentration of plasma LH in castrated, intact, fully fed, or fasted cockerels. Perifusion of mediobasal-preoptic hypothalami from castrated or intact cockerels with 200 microM naloxone or mediobasal hypothalami from fully fed or fasted cockerels with 10 microM naloxone failed to stimulate the release of LHRH-I. These observations suggest in the cockerel that endogenous opioid peptides may not play an obligatory role in the inhibitory control of the tonic secretion of luteinizing hormone.

Animals↗

Insulin-like growth factor-I stimulated growth and progesterone production by granulosa-lutein cells. Lack of interaction with physiological concentrations of luteinizing hormone and follicle stimulating hormone.

This study examined the effect of physiological concentrations of insulin-like growth factor-I (IGF-I), follicle stimulating hormone (FSH) and luteinizing hormone (LH) alone and in combination on growth and progesterone production by human granulosa-lutein cells. Granulosa-lutein cells were obtained from patients (n > 5) undergoing in-vitro fertilization (IVF) or gamete intra-Fallopian transfer (GIFT) treatment. Cells were cultured for 2 and 4 days in the presence of physiological concentrations of human LH (code 68/40, 5 IU/l), FSH (code 83/575, 20 IU/l), or IGF-I (30 ng/ml) alone and in combination. Medium was changed every 2 days. No change in cell number (relative to each patient's own control) was observed after treatment with FSH or LH alone or in combination at any time. IGF-I alone produced a 117 +/- 8% and 176 +/- 15% (mean +/- SEM, n = 5) increase in cell number after 2 and 4 days respectively. This increase was unaffected by the addition of LH or FSH at any time. Basal progesterone secretion was variable (1633, 975-2409 nmol/l, median and interquartile range, day 2) and decreased with time in culture (564, 375-1089 nmol/l, day 4). After 2 days culture progesterone output increased by 116 +/- 5% of control in response to LH and 153 +/- 13% (mean +/- SEM, n = 5) of control in response to IGF-I. After 4 days, LH and IGF-I stimulated progesterone levels by 279 +/- 52% and 264 +/- 37% (mean +/- SEM, n = 5) respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Androstenedione↗

Ovulatory response, and plasma concentrations of luteinizing hormone and progesterone following administration of synthetic mammalian or chicken luteinizing hormone-releasing hormone relative to the first or second ovulation in the sequence of the domestic hen.

Experiments were conducted to investigate hypophyseal and follicular competency at two distinct stages of the hen's egg laying sequence: 1) 14 h prior to the first (C1) ovulation of a sequence (27 h following the previous ovulation); and 2) 14 h prior to the second (C2) ovulation of a sequence (13 h following the previous ovulation). When a single dose of mammalian luteinizing hormone-releasing hormone (mLHRH) or chicken luteinizing hormone-releasing hormone (cLHRH) was injected 14 h prior to a C1 ovulation, premature ovulation was induced in 19 of 20 hens. In contrast, ovulation was premature in only 1 of 20 hens when mLHRH or cLHRH was injected 14 h prior to a C2 ovulation. There was no difference between the two stages of the sequence in the amount of luteinizing hormone (LH) released for up to 60 min following a single i.v. injection of 20 micrograms mLHRH. However, only prior to a C1 ovulation did LH levels further increase to reach preovulatory concentrations. By contrast, progesterone (P4) concentrations were increased within the first 60 min to a lesser extent in hens injected prior to a C2 ovulation compared to a C1 ovulation. In C2-injected birds, P4 fell to levels that were not different from vehicle-injected controls by 45 to 60 min following injection, whereas P4 secretion was maintained in hens injected prior to a C1 ovulation. We suggest that the lack of sustained LH secretion following treatment with either species of LHRH 14 h prior to a C2 ovulation is related to follicular immaturity with respect to ability to produce and secrete P4. At the dosage administered, there was no difference in the ability of mLHRH compared to cLHRH to release LH at either stage of the sequence. Finally, two successive injections of mLHRH at 14 and 13 h prior to a C2 ovulation induced premature ovulation in 6 of 11 hens. It is suggested that LH, and possibly P4, exerts a priming effect on the largest preovulatory follicle to initiate fully potentiated P4 production and secretion.

Animals↗

Luteinizing hormone induces prostaglandin endoperoxide synthase-2 and luteinization in vitro by A-kinase and C-kinase pathways.

The LH surge induces ovulation [prostaglandin synthase-2 (PGS-2)] and luteinization (progesterone synthesis) of preovulatory follicles by cAMP-dependent mechanisms. Peptides, such as GnRH and angiotensin-II, that activate other cellular signaling pathways have been shown to mimic some of the effects of LH. Therefore, the relative functional importance of different cellular signaling pathways in mediating the induction of PGS-2 and luteinization was analyzed using the agonists (LH, GnRH, and angiotensin-II) and selective inhibitors of A-kinase (H-89), C-kinase (calphostin-C), and calmodulin kinase-II (KN93). LH or GnRH, but not angiotensin-II, markedly induced PGS-2 protein in preovulatory follicles. H-89 and calphostin-C, but not KN93 inhibited LH induction of PGS-2, whereas calphostin-C selectively blocked induction by GnRH. In contrast, the A- and C-kinase inhibitors prevented both LH and GnRH induction of granulosa cell luteinization. Taken together, these results provide biological evidence that the response of granulosa cells to the LH surge appears to involve the activation of A- and C-kinase pathways.

Animals↗

Induction of luteinized unruptured follicles in the rat after injection of luteinizing hormone early in pro-oestrus.

The cause of formation of luteinized unruptured follicles (LUF) is unknown. Formation of LUF was studied after injection of a varying small dose of luteinizing hormone (LH) with or without subsequent injection of gonadotrophin-releasing hormone (GnRH); in addition, the effect of suppression of prolactin on LUF formation was studied. Luteinization without ovulation occurred in virtually all graafian follicles, if 0.5-1.0 microgram of LH was injected some hours before the presumed endogenous LH surge (suppressed by Nembutal); with increasing doses of LH progressively increasing numbers of ovulations were observed. If an early pro-oestrus 1 microgram of GnRH was given 4 h after 1 microgram of LH, formation of LUF was partly prevented; if the interval between LH and GnRH was 8 h or more, the great majority of graafian follicles developed into LUF. If early in pro-oestrus 1 microgram of LH was given and 8 h later 0.1 microgram of a potent GnRH analogue, about 50% of the follicles became LUF; in similarly treated rats, suppression of prolactin by ergocryptine reduced but did not prevent LUF formation. The data support the idea that deficient LH secretion in the period before ovulation may be involved in the formation of LUF.

Animals↗

Cyclic release of luteinizing hormone and the effects of luteinizing hormone-releasing hormone injection in Asiatic elephants.

Cyclic changes in serum concentration of luteinizing hormone (LH) were observed throughout the estrous cycle of Asiatic elephants (Elephas maximus). The increase in serum LH was correlated with a slight increase in serum estradiol concentration and the onset of behavioral heat (willingness to mate). In a second series of studies, injection of luteinizing hormone-releasing hormone after 3 days of estrone administration induced an increase in serum LH. These studies indicate that the Asiatic elephant exhibits a cyclic LH release that can be experimentally induced by estrone and luteinizing hormone-releasing hormone administration.

Animals↗

Hypothalamic luteinizing hormone-releasing hormone content and serum luteinizing hormone levels in male rats during wallerian degeneration of sympathetic nerve terminals after superior cervical ganglionectomy.

The main hypothesis of this study was that sympathetic neurons located at the superior cervical ganglia (SCG) control luteinizing hormone (LH) releasing mechanisms by acting at a hypothalamic site. To test this, medial basal hypothalamus (MBH) luteinizing hormone-releasing hormone (LHRH) content and serum LH levels were measured in male rats subjected to superior cervical ganglionectomy (SCGx) or sham-operation 14 or 38 h earlier, at the time of degeneration of nerve endings post-SCGx. Significantly augmented MBH LHRH levels and decreased circulating LH were found in SCGx rats. In animals subjected to SCGx 14 h earlier and receiving a single injection of the alpha 1-adrenergic blocker prazosin, the beta-adrenergic blocker propranolol or a mixture of both drugs 45 min before sacrifice, only the injection of prazosin prevented the decrease of plasma LH levels. Neither treatment prevented the increase in MBH LHRH content. When prazosin was given every hour starting from the 10th to the 13th h after surgery, it was effective to prevent both the increase of MBH LHRH content and the decrease of serum LH found during sympathetic nerve degeneration. Similar repetitive injections of propranolol resulted in the greatest depression of serum LH, and in the greatest increase of MBH LHRH observed. Serum LH response to LHRH injection was similar in SCGx and sham-operated rats. The data indicate that SCG neurons exert, through inhibitory alpha 1-, and weaker, stimulatory beta-adrenoceptors, a significant influence on LHRH release at a supra-hypophysial site.

Animals↗

On the correlation of luteinizing hormone-releasing hormone, luteinizing hormone, follicle-stimulating hormone, and prolactin levels in plasma of women with normal menstrual cycles.

During seven follicular, five periovulatory, and seven luteal days of the menstrual cycle, concentrations of luteinizing hormone-releasing hormone (LHRH), luteinizing hormone (LH), follicle-stimulating hormone (FSH), prolactin (PRL), total estrogen (TE), and progesterone (P) were measured every 20 minutes over a 3 or a 5 hour period in samples of venous plasma obtained from women with normal menstrual cycles. Episodic peaks of LHRH, LH, and PRL and less pronounced elevations of FSH were observed. Correlation analysis of the study demonstrated the following: (1) During early follicular and late luteal days, a synchrony was observed between LHRH and LH pulses and trends. There was a positive correlation between LHRH and LH levels only during the early follicular days (p less than 0.05), demonstrating a probable LHRH control of LH release. (2) When TE and TE/P concentrations increased during the late follicular and early luteal days, respectively, no correlation was present between LHRH and LH levels and trends. (3) Neither a synchrony nor a correlation was detectable between LHRH and FSH pulses or levels during any of the cycle days. (4) A statistical correlation existed between LH and PRL concentrations during various days of the cycle, more specifically during the periovulatory period, suggesting a common release mechanism for these two pituitary hormones.

Adult↗