Patterns of spontaneous LH release in normo- and hyperprolactinaemic women

1981 ◽  
Vol 97 (3) ◽  
pp. 305-310 ◽  
Author(s):  
Maire T. Buckman ◽  
Glenn T. Peake ◽  
Laxima Srivastava ◽  
Josephine Morris ◽  
Barry David ◽  
...  
Keyword(s):  
Sampling Period ◽  
Normal Subjects ◽  
Plasma Prolactin ◽  
Early Follicular Phase ◽  
Lh Release ◽  
Normal Women ◽  
17 Hydroxyprogesterone ◽  
Group Sex ◽  
Lh Secretion

Abstract. Hyperprolactinaemia may be associated with functional amenorrhoea. In order to evaluate the possible role of abnormal spontaneous LH secretion in hyperprolactinaemic amenorrhoeic women, plasma LH was measured at 15 min intervals for 300 min in 12 normal women during the early follicular phase of the menstrual cycle and compared to that observed in 11 hyperprolactinaemic amenorrhoeic subjects. Mean plasma prolactin was 9.1 ± 3.6 ng/ml (x̄ ± sem) in the euprolactinaemic and 168 ± 32 ng/ml in the hyperprolactinaemic group. Sex steroids including oestrone, oestradiol, progesterone and 17-hydroxyprogesterone were similar in the 2 groups. Mean plasma LH levels over the 300 min sampling period were 9.4 ± 1.6 mIU/ml in the normal subjects and 7.5 ± 1.0 mIU/ml in the hyperprolactinaemic patients (P>0.10). Every normal woman exhibited at least one LH spike in excess of 10 mIU/ml. Five hyperprolactinaemic patients failed to exhibit any LH spikes above 10 mIU/ml (P < 0.02 compared to controls). Thus, hyperprolactinaemia was associated with an absence of LH spike activity in 45% of patients studied and this abnormality may play an aetiologic role in the hypogonadism observed in these subjects; in those hyperprolactinaemic subjects with pulsatile LH secretion, however, other explanations for their amenorrhoea should be considered.

Interaction of dopaminergic and antiserotoninergic drugs in the control of prolactin and LH release in normal women

1980 ◽  
Vol 93 (3) ◽  
pp. 271-276 ◽  
Author(s):  
Antonio E. Pontiroli ◽  
Miriam Alberetto ◽  
Gabriele Pellicciotta ◽  
Emilio De Castro e Silva ◽  
Anna De Pasqua ◽  
...  
Keyword(s):  
Experimental Animal ◽  
Lh Surge ◽  
Inhibiting Effect ◽  
Lh Release ◽  
Normal Women ◽  
Plasma Prl ◽  
Lh Secretion

Abstract. Prolactin (Prl) release, both in the experimental animal and in man, is stimulated by serotonin (5HT) and inhibited by dopamine (DA). Data also suggest that LH release in the animal is stimulated by norepinephrine and inhibited by DA. The role of 5HT in the control of LH release is less clear. It would appear to stimulate episodic LH release and to inhibit the LH surge at the pro-oestrus in animals, but the effect of 5HT on LH release has not yet been evaluated in man. In the present paper we have studied the effect of various DA-ergic drugs (DA, iv 1-dopa, po 1-dopa and bromoergocriptine) and of two anti-5HT drugs, metergoline and methysergide, on Prl and LH release in normal women. DA-ergic drugs lowered plasma Prl and LH levels; anti-5HT drugs, at doses able to lower Prl levels, did not affect basal LH release nor the inhibiting effect of iv 1-dopa on LH release. These data indicate that DA inhibits both LH and Prl release in normal women, and that 5HT stimulates Prl release but is not involved in the regulation of LH secretion. The fact that, at variance to all the DA-ergic drugs used, the two anti-5HT drugs did not vary LH release, suggests that metergoline and methysergide are devoid of DA-ergic activity in man, at least at the doses able to inhibit Prl release.

Histamine-induced paradoxical GH response to TRH/GnRH in men and women: Dependence on gonadal steroid hormones

1990 ◽  
Vol 122 (3) ◽  
pp. 354-360 ◽  
Author(s):  
Ulrich Knigge ◽  
Benedikte Thuesen ◽  
Anders Dejgaard ◽  
Birgit Svenstrup ◽  
Paul Bennett
Keyword(s):  
Menstrual Cycle ◽  
Luteal Phase ◽  
Normal Subjects ◽  
Gh Secretion ◽  
Early Follicular Phase ◽  
Estrone Level ◽  
Normal Women ◽  
Two Phases ◽  
Normal Men

Abstract A stimulatory GH response to TRH and GnRH occurs frequently in patients with various pathological conditions, but is absent in normal subjects. We have previously shown that histamine induced a paradoxical GH response to TRH in normal men. Since gonadal steroids influence GH secretion, we investigated whether infusion of histamine might induce a GH response to combined administration of TRH (200 μg) and GnRH (100 μg) in 6 normal women during the early follicular and luteal phase of the same menstrual cycle and in 7 normal men. Histamine had no effect on basal GH secretion in men or in women during the two phases of the menstrual cycle. However, compared with saline, histamine induced a GH response to TRH/GnRH in men (GH peak: 5.5 ± 1.0 vs 1.4 ± 0.3 μg/l; p<0.01) and in women during the luteal phase (GH peak: 5.2 ± 1.6 vs 1.5 ± 0.4 μg/l; p<0.025), but not during the early follicular phase of the cycle (GH peak: 1.7 ± 0.5 vs 1.6 ± 0.3 μg/l). In luteal-phase women the GH response to TRH/GnRH correlated with the serum estradiol-17β level (GH area/E2: r=0.98; p<0.005) and the serum estrone level (GH area/E1: r=0.81; p<0.05). In men the GH response to TRH/GnRH did not correlate with estrogen or androgen levels. We conclude that high physiological levels of estrogens are pertinent to the activation of a histamine-induced GH response to TRH/GnRH in women, whereas the role of androgens and estrogens for the induction of the response in men seems more complex. Furthermore, the study indicates that histamine may increase the sensitivity of GH release to nonspecific stimuli.

Involvement of norepinephrine in pituitary LH release induced by oestradiol in vitro

1984 ◽  
Vol 107 (2) ◽  
pp. 199-203
Author(s):  
A. Miyake ◽  
K. Tasaka ◽  
T. Aono
Keyword(s):  
Oestrous Cycle ◽  
Female Rats ◽  
Direct Effects ◽  
Significant Release ◽  
Lh Release ◽  
Lh Secretion ◽  
Perifusion System ◽  
Double Chamber

Abstract. The direct effects of oestradiol-17β (E2) on pituitary luteinizing hormone (LH) release and the role of norepinephrine (NE) in E2-induced gonadtrophin release were examined in a sequential double chamber perifusion system by perifusing the mediobasal hypothalami (MBH) and/or pituitaries excised from normally cycling female rats. Administration of E2 induced significant release (70–160% increase, P < 0.05) of LH from the pituitary of rats in pro-oestrus, but not in other stages of the oestrous cycle. When the MBH and the pituitary were perifused in sequence, E2 induced significant release of LH in all stages of the oestrous cycle except oestrus. When the pituitary from rats in dioestrus II was perifused alone with medium containing 200 ng/ml NE, significant release of LH (80–170% increase, P < 0.05) was observed after the administration of E2. The E2-induced LH release in pro-oestrus was completely abolished by perifusion with medium containing diethyldithiocarbamate, an inhibitor of NE synthesis. These findings suggest that NE may be involved in changes of pituitary responsiveness in LH secretion to oestrogen during the rat oestrous cycle.

scholarly journals Characterization of the Role of NKA in the Control of Puberty Onset and Gonadotropin Release in the Female Mouse

Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2453-2463 ◽  
Author(s):  
Silvia León ◽  
Chrysanthi Fergani ◽  
Rajae Talbi ◽  
Serap Simavli ◽  
Caroline A Maguire ◽  
...  
Keyword(s):  
Sex Steroids ◽  
Neurokinin A ◽  
Central Control ◽  
Gnrh Release ◽  
Lh Release ◽  
Timing Of Puberty ◽  
Puberty Onset ◽  
Lh Secretion

Abstract The tachykinin neurokinin B (NKB, Tac2) is critical for proper GnRH release in mammals, however, the role of the other tachykinins, such as substance P (SP) and neurokinin A (NKA) in reproduction, is still not well understood. In this study, we demonstrate that NKA controls the timing of puberty onset (similar to NKB and SP) and stimulates LH release in adulthood through NKB-independent (but kisspeptin-dependent) mechanisms in the presence of sex steroids. Furthermore, this is achieved, at least in part, through the autosynaptic activation of Tac1 neurons, which express NK2R (Tacr2), the receptor for NKA. Conversely, in the absence of sex steroids, as observed in ovariectomy, NKA inhibits LH through a mechanism that requires the presence of functional receptors for NKB and dynorphin (NK3R and KOR, respectively). Moreover, the ability of NKA to modulate LH secretion is absent in Kiss1KO mice, suggesting that its action occurs upstream of Kiss1 neurons. Overall, we demonstrate that NKA signaling is a critical component in the central control of reproduction, by contributing to the indirect regulation of kisspeptin release.

Alterations of the hypothalamic GnRH interpulse interval sequence over the normal menstrual cycle

1988 ◽  
Vol 255 (5) ◽  
pp. E696-E701 ◽  
Author(s):  
N. Santoro ◽  
J. P. Butler ◽  
M. Filicori ◽  
W. F. Crowley
Keyword(s):  
Menstrual Cycle ◽  
Renewal Process ◽  
Gnrh Secretion ◽  
Late Luteal Phase ◽  
Normal Menstrual Cycle ◽  
Lh Release ◽  
Interval Sequence ◽  
Normal Women ◽  
Normal Men ◽  
Lh Secretion

Luteinizing hormone (LH) is released in a pulsatile fashion from the anterior pituitary in response to hypothalamic gonadotropin-releasing hormone (GnRH) secretion. Previous autocorrelation analysis of the sequence of interpulse intervals of LH secretion in normal men has supported the hypothesis that the underlying hypothalamic mechanism of GnRH secretion governing episodic LH release is a renewal process, indicating that hypothalamic "memory," if present, does not extend back further in time than the preceding secretory pulse. A similar analysis of pulsatile LH secretion was undertaken in 45 studies of normal women, obtained throughout the menstrual cycle. Analysis of these studies revealed a process consistent with renewal throughout the follicular and early luteal phases. However, this relationship appears to break down in the mid-to-late luteal phase, indicating that alternative feedback pathways provide an overriding influence on the underlying renewal process of hypothalamic GnRH secretion. Pulsatile progesterone secretion by the corpus luteum, which first emerges at this stage of the menstrual cycle, may be the agent responsible for this feedback.

Adrenal progesterone facilitates the negative feedback of oestrogen on LH release in ovariectomized rats

1993 ◽  
Vol 139 (2) ◽  
pp. 253-258 ◽  
Author(s):  
A. M. Salicioni ◽  
R. W. Carón ◽  
R. P. Deis
Keyword(s):  
Ovariectomized Rats ◽  
Adrenal Steroids ◽  
Serum Progesterone ◽  
Oestrogen Treatment ◽  
Ovx Rats ◽  
Serum Lh ◽  
Oestradiol Benzoate ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT There is evidence that the adrenals play a role in the regulation of the synthesis and release of gonadotrophins in various vertebrates. The aim of this study was to determine the part played by adrenal steroids, with special reference to progesterone, on the concentration of LH in ovariectomized (OVX) and oestrogen-primed rats. OVX rats received a single s.c. injection of vehicle or oestradiol benzoate (OB, 20 μg/rat). This day was designated as day 0. Three or four days later (day 3–day 4), the rats were treated with mifepristone (10 mg/kg) or with two doses of progesterone antiserum and blood samples were obtained at 13.00 and 18.00 h. OB treatment of OVX rats reduced serum LH at 13.00 h and 18.00 h on day 3 but only at 13.00 h on day 4. The administration of mifepristone at 08.00 h to OVX and oestrogen-treated rats induced a significant increase in serum LH at 18.00 h on days 3 and 4, without modifying the values at 13.00 h. When mifepristone was given at 13.00 h a much larger increase in serum LH was obtained at 18.00 h. In OVX and oestrogen-treated rats, adrenalectomy on day 2 (08.00–09.00 h) induced an increase in serum LH at 18.00 h similar to that observed in the OVX and oestrogen-primed rats after mifepristone treatment. In order to determine the specificity of the effect of mifepristone, a group of OVX and oestrogentreated rats was injected with progesterone antiserum at 08.00 and 13.00 h on day 3. Serum LH concentrations at 13.00 and 18.00 h on day 3 were similar to values obtained in OVX rats treated with oestrogen and mifepristone. Serum progesterone was measured at 08.00 and 13.00 h in OVX and OVX and oestrogenprimed rats. At both times, values were similar in OVX rats but oestrogen treatment significantly increased serum progesterone levels. The important role of adrenal progesterone on the regulation of LH secretion in OVX and oestrogen-primed rats is evident from these results. Blocking progesterone action at the receptor level, we showed that OB significantly increased LH values at 18.00 h. On the basis of these studies it is tempting to speculate on the possibility of an inhibitory or stimulatory effect of oestrogen on serum LH concentration in OVX rats, according to the presence or absence of adrenal progesterone action. Journal of Endocrinology (1993) 139, 253–258

Role of prolactin in age-related change in serum dehydroepiandrosterone sulphate concentrations

1989 ◽  
Vol 120 (5) ◽  
pp. 655-660 ◽  
Author(s):  
Tohru Yamaji ◽  
Miyuki Ishibashi ◽  
Fumimaro Takaku ◽  
Akira Teramoto ◽  
Kintomo Takakura ◽  
...  
Keyword(s):  
Elevated Serum ◽  
Normal Subjects ◽  
Significant Negative Correlation ◽  
Adrenocortical Function ◽  
Dehydroepiandrosterone Sulphate ◽  
Age Related ◽  
Number Of Patients ◽  
Normal Women

Abstract. Serum dehydroepiandrosterone sulphate concentrations were measured in 70 patients with prolactinoma and in 54 patients with acromegaly with normal adrenocortical function. Compared with values in normal subjects of corresponding age, serum dehydroepiandrosterone sulphate levels were increased in 22 patients with prolactinoma (31%) and in 5 patients with acromegaly (9%). The four acromegalic patients who had elevated serum dehydroepiandrosterone sulphate levels had hyperprolactinemia. The mean serum dehydroepiandrosterone sulphate concentrations in patients with prolactinoma in each decade decreased with advancing age. There was a significant negative correlation between serum dehydroepiandrosterone sulphate concentrations and ages of the patients with prolactinoma. In all 8 women with prolactinoma as in 6 normal women, serum dehydroepiandrosterone sulphate levels declined definitely during the 9 years of follow-up despite persistent hyperprolactinemia. These results indicate that serum dehydroepiandrosterone sulphate levels are increased in a substantial number of patients with hyperprolactinemia, however, PRL per se may not play a significant role in the age-related change in serum dehydroepiandrosterone sulphate levels.

Suppressed plasma prolactin response to thyrotropin-releasing hormone in hyperthyroidism reproduced by thyroxine but not by triiodothyronine administration to normal subjects

1988 ◽  
Vol 117 (2) ◽  
pp. 241-248 ◽  
Author(s):  
Eva Marie Erfurth ◽  
Pavo Hedner
Keyword(s):  
Control Level ◽  
Normal Subjects ◽  
Sex Hormone Binding Globulin ◽  
Plasma Prolactin ◽  
Serum Free ◽  
Basal Plasma ◽  
Normal Women ◽  
Prolactin Response ◽  
Plasma Prl ◽  
Hyperthyroid Patients

Abstract. In 10 hyperthyroid women studied in the follicular phase of the menstrual cycle, basal plasma PRL was normal, but PRL release after TRH was significantly suppressed compared with that in 11 control women. The suppressed PRL response to TRH was not explained by changes in serum estradiol or sex hormone-binding globulin. It recovered after treatment of hyperthyroidism. When normal women were treated with T4 (0.5 mg daily for 6 to 10 days), their mean serum free T4 level increased to about 70% of that in the hyperthyroid patients, whereas their serum free T3 levels increased to a lesser degree. During T4 administration, these women had PRL changes similar to those of the hyperthyroid patients. When the normal women took T3 (60–120) μg for 6 to 8 days), their serum free T3 increased to almost the level of the hyperthyroid patients, but the TRH stimulated PRL release remained close to the control level. The PRL increase after dopaminergic blockade with metoclopramide was significantly suppressed in hyperthyroid patients, and they had no PRL response to TRH after pretreatment with metoclopramide. In conclusion, the PRL changes in hyperthyroidism were reproduced by administration of T4, but not by administration of T3 to healthy women. The site of action is suggested to be pituitary, but additional hypothalamic effects cannot be excluded.

Fasting impairs LH secretion in female rats by activating an inhibitory opioid pathway

1985 ◽  
Vol 105 (1) ◽  
pp. 91-97 ◽  
Author(s):  
R. G. Dyer ◽  
S. Mansfield ◽  
H. Corbet ◽  
A. D. P. Dean
Keyword(s):  
Sampling Period ◽  
Significant Rise ◽  
Female Rats ◽  
Opioid Antagonist ◽  
Endogenous Opioid ◽  
Opioid Mechanisms ◽  
Before And After ◽  
Naloxone Hydrochloride ◽  
Lh Release ◽  
Lh Secretion

ABSTRACT Two experiments were undertaken to investigate the way that fasting impairs LH secretion and to assess whether endogenous opioid mechanisms might be responsible for the impairment. In the first experiment, pulsatile LH secretion was measured in a total of 51 chronically ovariectomized female rats. Initially 29 rats were subjected to food withdrawal for 24, 48, 72 or 120 h before the experiment. When compared with data collected from eight unfasted control rats, the 120-h fast was found to reduce significantly the mean peak and trough values of the LH pulses measured. However, in a subsequent study, the inhibition of pulsatile LH secretion by a 120-h fast was prevented in a group of eight rats given the opioid antagonist naloxone hydrochloride before the start of the blood-sampling period. Naloxone was without effect on pulsatile LH secretion in eight unfasted control rats. In the second experiment, plasma LH concentrations were measured before and after unilateral electrical stimulation of the ventral noradrenergic tract (VNAT) in ovariectomized female rats pretreated with oestradiol benzoate. In 17 rats VNAT stimulation caused a significant rise in plasma LH, but after a 72-h fast this rise was significantly less than in unfasted control rats. However, pretreatment of fasted rats with naloxone (n = 9) significantly enhanced the VNAT-stimulated release of LH to the control values. Naloxone did not potentiate VNAT-stimulated LH release in unfasted animals (n = 6) or LH release in control unstimulated rats (n = 12). The experiments indicate that both pulsatile LH secretion, and LH release caused by VNAT stimulation, are impaired by an acute fast. In both cases, the impairment is prevented by pretreatment with naloxone. Thus fasting probably activates an inhibitory opioid pathway within the brain to inhibit LH secretion. J. Endocr. (1985) 105, 91–97

Episodic nyctohemeral secretion of melatonin in adult humans: Lack of relation with LH pulsatile pattern

1990 ◽  
Vol 122 (1) ◽  
pp. 76-82 ◽  
Author(s):  
Alberto de Leiva ◽  
Federico Tortosa ◽  
Miguel A. Peinado ◽  
José Serrano ◽  
José Rodriguez-Espinosa ◽  
...  
Keyword(s):  
Mean Amplitude ◽  
Melatonin Secretion ◽  
Melatonin Concentration ◽  
Significant Difference ◽  
Adult Humans ◽  
Early Follicular Phase ◽  
The Mean ◽  
Normal Women ◽  
Normal Men ◽  
Lh Secretion

Abstract The concentration of melatonin and LH were determined in plasma samples obtained at 10-min intervals during 4 h of darkness (00.00-04.00 h) from 4 normal women, age 23-27 years, in the early follicular phase of the menstrual cycle and in 6 normal men, age 23-31 years. Additionally, melatonin concentration was determined in samples obtained from the men at 10-min intervals for 4 h during the day (10.00-14.00 h). A pulsatile pattern of melatonin secretion was found for all the subjects during darkness. There was no significant difference between women and men as to the number of pulses (2.8 ± 0.5 vs 5.2 ± 1.0 per 4 h), amplitude of pulses (51.3 ± 28 vs 27.2 ± 6 ng/l), concentration per 4 h (32.5 ± 13 vs 31.0 ± 5 ng/l), or apparent half-life of melatonin (19.3 ± 2.3 vs 15.3 ± 7.5 min). The mean amplitude of the melatonin pulse correlated (r = 0.863, p<0.001) with the mean melatonin concentration per 4 h. A pulsatile LH secretion pattern was found for the 10 subjects and did not correlate significantly with the melatonin secretion pattern. The results are consistent with an independent signal for the demonstrated nyctohemeral pulsatile melatonin and LH secretions.

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