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PubMed1978

Pituitary hormone control of implantation in the mouse.

In hypophysectomized pregnant mice replacement therapy designed to mimic the normal physiological situation showed that FSH in combination with either prolactin or LH, or prolactin plus LH, could initiate implantation in the absence of the pituitary gland. No pituitary hormone was by itself capable of achieving this result. The combination of prolactin with FSH gave better results than a combination of LH with FSH. Prolactin from sheep, cattle or rats was equally effective in combination with rat FSH in initiating implantation. In mice exhibiting suckling-induced delay of implantation this delay was terminated by injection of FSH. GH by itself or in conjunction with other hormones had no significant effect on implantation or on any of the other parameters associated with implantation that were measured. On the basis of these experimental results it is suggested that prolactin and LH are involved with progesterone production and FSH with oestrogen production, both of which are required for implantation in the mouse.

Animals↗
PubMed1984

Lack of inhibition of anterior pituitary hormone release during chronic treatment with calcium antagonists.

Calcium antagonists are widely used for the treatment of cardiovascular disorders, especially ischaemic heart disease. It has been demonstrated that these drugs, either in vitro or acutely administered in humans, inhibit the basal and stimulated secretion of pituitary hormones by blocking calcium influx through slow calcium channels. To see if a similar effect could be detected after their chronic administration, we studied the basal, TRH- and LHRH-stimulated TSH, PRL, LH and FSH release in 18 male subjects with chronic stable angina before and on the 30th day of oral treatment with verapamil (n = 8;80 mg three times a day) or with nifedipine (n = 10; 10 mg three times a day). Neither drug had any effect on basal TSH, PRL, LH and FSH values or on their response to the specific hypothalamic-releasing hormones. These results suggest that the chronic administration of calcium antagonists, at the usual therapeutic doses, does not effect the process of stimulus-secretion coupling of anterior pituitary hormones, ruling out any impairment of the related target glands which have been expected on the basis of previous studies.

Aged↗
PubMed2005

Novel mutations within the POU1F1 gene associated with variable combined pituitary hormone deficiency.

CONTEXT: Mutations within the gene encoding the pituitary-specific transcription factor POU1F1 are associated with combined pituitary hormone deficiency (CPHD). Most of the affected individuals manifest GH, prolactin, and TSH deficiency. OBJECTIVE: We have now screened 129 individuals with CPHD and isolated GH deficiency for mutations within POU1F1. RESULTS: Causative mutations were identified in 10 of 129 individuals (7.8%). Of these, five patients harbored the dominant negative R271W mutation, which is a well-recognized mutational hot spot. We have also identified a second frequently occurring mutation, E230K, which appears to be common in Maltese patients. Additionally, we describe two novel mutations within POU1F1, an insertion of a single base pair (ins778A) and a missense mutation (R172Q). Functional studies have revealed that POU1F1 (E230K) is associated with a reduction in transactivation, although DNA-binding affinity is similar to the wild-type protein. On the other hand, POU1F1 (R172Q) is associated with a reduction in DNA binding and transactivation, whereas POU1F1 (ins778A) is associated with loss of DNA binding and a reduction in transactivation. CONCLUSIONS: Our data suggest that the phenotype associated with POU1F1 mutations may be more variable, with the occasional preservation of TSH secretion. Additionally, our data revealed POU1F1 mutations in three patients who were diagnosed as having ACTH deficiency but who, on further evaluation, were found to have normal cortisol secretion. Hence, elucidation of the genotype led to further evaluation of the phenotype, with the cessation of cortisol replacement that had been commenced unnecessarily. These data reflect the importance of mutational analysis in patients with CPHD.

Amino Acid Sequence↗
PubMed1993

Acute effects of cocaine on anterior pituitary hormones in male and female rhesus monkeys.

The effects of acute cocaine administration (0.4 or 0.8 mg/kg) on anterior pituitary hormones were studied in four male and six female adult rhesus monkeys during the midluteal phase of the menstrual cycle (days 20-23). Progesterone levels averaged 15.7 +/- 3 and 10.6 +/- 2.8 ng/ml before low and high dose cocaine administration. Integrated plasma samples were collected every 10 min for 40 min before i.v. administration of cocaine, and 11 postcocaine samples were collected over 110 min. Cocaine (0.8 mg/kg) stimulated a significant increase in luteinizing hormone (LH) within 10 to 20 min (P < .01) and LH reached peak levels (59-60% above base line) within 30 min after cocaine administration in both males and females. Plasma cocaine levels averaged 289 +/- 23 and 346 +/- 73 ng/ml at 10 min after i.v. cocaine (0.8 mg/kg) administration in males and females, respectively. Follicle stimulating hormone levels were unchanged in midluteal females. Male testosterone increased by 50% above average base-line levels 50 min after the LH peak (80 min postcocaine). These data are consistent with our previous findings that cocaine increased LH and enhanced luteinizing hormone-releasing hormone-stimulated LH in early follicular females. The low dose of cocaine did not change basal levels of LH and follicle stimulating hormone in midluteal females and both LH and testosterone were unaffected in males. Cocaine plasma levels averaged 97.6 +/- 29 and 68.3 +/- 9.1 ng/ml at 10 min after 0.4 mg/kg of cocaine in males and females, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

Normal pituitary hormone response to thyrotrophin and gonadotrophin releasing hormones in subjects exposed to elemental mercury vapour.

Exposure to elemental mercury (Hg) vapour results in an accumulation of Hg in the pituitary, the thyroid, and the testis. In this study, basal serum concentrations of pituitary hormones (thyrotrophin (TSH), prolactin (PRL), follicle stimulating hormone (FSH), and luteinising hormone (LH] or their response after administration of thyrotrophin and gonadotrophin releasing hormones did not differ between 11 male workers (mean urinary Hg (U Hg) concentration 26 nmol/mmol creatinine) and nine male dentists (U Hg concentration 1.3 nmol/mmol creatinine) exposed to elemental Hg vapour when compared with matched referent groups (U Hg concentration 0.6 and 0.4 nmol/mmol creatinine). Thus there was no evidence of an effect of Hg on the pituitary. Neither was there any association between exposure to Hg and serum concentrations of free thyroid hormones (S FT3, S FT4), testosterone, or cortisol. Increased plasma concentrations of selenium (Se) were associated with increased basal serum concentrations of TSH, decreased concentrations of basal serum cortisol, and decreased release of FSH.

Adult↗
PubMed1999

Effects of neuropeptide Y (NPY), galanin and vasoactive intestinal peptide (VIP) on pituitary hormone release and on ovarian steroidogenesis.

Ovarian folliculogenesis is regulated by the gonadotrophins, but in recent years other peptides have been found to serve as local regulators of ovarian function. The aim of this study is to evaluate the effects of NPY, galanin and VIP on pituitary and gonadal hormone release. Effects of NPY, galanin and VIP on progesterone, estradiol production by cultured rat granulosa and effects of these peptides on pituitary hormone release by cultured pituitary cells were examined according to methods previously described. Maximal effects of NPY, galanin and VIP on pituitary hormone release and on gonadal steroids were observed after administration of 10 nM of these peptides during 60 mins incubation. VIP and NPY, but not galanin, stimulated PRL release from cultured pituitary cells. VIP increased also LH release whenever NPY and galanin did not change LH release from pituitary cells. Galanin, but not NPY and VIP, leads to an increase of GH production. VIP, NPY and galanin did not change TSH and FSH release. NPY, galanin and VIP markedly stimulated progesterone release from cultured granulosa cells. NPY, galanin and VIP did not change estradiol and testosterone release. Conclusions. Direct effects of NPY, galanin and VIP on pituitary hormone release may indicate their role in the mechanism of pituitary hormone release. A marked increase of progesterone from cultured granulosa cells after VIP, NPY and galanin suggests that these peptides may be involved in the local ovarian steroidogenesis.

Journal Article↗
PubMed1998

Bright light exposure and pituitary hormone secretion.

OBJECTIVE: Exposure to bright light inhibits melatonin secretion in man. As the relationship between melatonin and pituitary function remains controversial, we investigated the effect of altering the melatonin rhythm by bright light during the early hours of darkness on pituitary hormone secretion in man. DESIGN: The investigation took the form of a randomized controlled clinical trial. SUBJECTS: Ten adult healthy male volunteers, who were non-smokers and aged 21-33 years, were studied on two occasions: once during exposure to bright light from 2000 h to 0200 h and once during exposure to normal room lighting over the same period. On each day of the study, the subjects were allowed to sleep after lights were switched off at 0200 h. Observations were also performed when subjects were exposed to normal room lighting from 2000 h to 2400 h, thereafter being allowed to sleep. On each study day the subjects undertook their normal duties but refrained from taking heavy exercise and drinking alcohol. MEASUREMENTS: Serum cortisol, GH and PRL, plasma vasopressin, oxytocin, melatonin, sodium, potassium and osmolality and packed cell volume were measured over 24 hours. RESULTS: Bright light delayed the nocturnal melatonin peak by 2 hours and resulted in a decrease in cortisol concentrations. Growth hormone levels decreased but subsequently there was a significantly greater nocturnal increase. The PRL peak was delayed and nocturnal vasopressin concentrations were lower in both the studies where subjects were exposed to a modified sleep schedule. CONCLUSION: Exposure to bright light during the early hours of darkness delays the nocturnal melatonin peak and alters cortisol, GH, PRL and nocturnal vasopressin secretion, while modification of the sleep pattern decreases vasopressin concentrations and alters its nocturnal peak.

Adult↗
PubMed1977

The effects of oral melatonin on skin color and on the release of pituitary hormones.

We studied the effects of prolonged ingestion of melatonin, 1 g per day, on skin color and the serum levels of pituitary hormones in 5 human subjects with hyperpigmented skin. Melatonin lightened hyperpigmented skin of one patient with untreated adrenogenital syndrome, but had no effect on three patients' skin with idiopathic hyperpigmentation and one patient with treated Addison's disease. Melatonin appeared to depress the level of luteinizing hormone (LH) in serum and may have inhibited in some patients the release of growth hormone from the pituitary gland after stimulation by stress or L-dopa. The subjects all noted increased drowsiness but through studies on the eyes, liver, kidneys, and bone marrow revealed no other evidence of toxicity.

17-Hydroxycorticosteroids↗
PubMed2000

Central hypocortisolism as part of combined pituitary hormone deficiency due to mutations of PROP-1 gene.

BACKGROUND: One of the causes of combined pituitary hormone deficiency (CPHD) is represented by Prophet of Pit-1 (PROP-1) gene inactivating mutations. This disorder is generally characterized by GH, TSH, prolactin (PRL), and gonadotropin deficiency, but recent papers have described a concomitant alteration of the corticotrope function. OBJECTIVE: To make a detailed investigation of the hypothalamic-pituitary-adrenal axis in two sisters with PROP-1 gene mutations. PATIENTS: Two female siblings (17 and 16 years old) with CPHD, belonging to a Brazilian family of consanguineous parents, presented with growth retardation and central hypothyroidism during childhood, and showed central hypogonadism at the age of puberty. No clear clinical symptoms and signs of hypocortisolism were present. METHODS: GH, TSH, free thyroxine, total tri-iodothyronine, PRL, LH, FSH, ACTH and cortisol were measured in basal condition and after appropriate testing. The molecular study was performed by PCR amplification and sequencing analysis of PROP-1 gene. RESULTS: Both patients showed GH, PRL, LH and FSH deficiencies, associated with absent responses to an insulin tolerance test (ITT), TRH and GnRH injection. Circulating concentrations of TSH were normal in basal conditions, but failed to respond to a TRH test. Plasma ACTH concentrations were normal, but serum cortisol concentrations were below the lower limit of the normal range, showing a trend to decrease during 6 years of follow-up. The serum ACTH response to ITT was impaired, whereas its response to CRH was normal and prolonged. The cortisol response to both tests, and to the ACTH test, was clearly impaired. In both sisters, the genetic analysis showed the presence of a homozygous 2-bp deletion (296delGA) of PROP-1 gene, which results in the synthesis of a protein with no residual functional activity. CONCLUSION: In addition to GH, TSH, PRL and gonadotropin deficiency, patients with PROP-1 gene mutations can present with late-onset central hypocortisolism, possibly beause of the lack of important paracrine factors normally produced by the cells surrounding the corticotropes and absent in the pituitary of these patients, or because of progressive corticotrope apoptosis. This finding indicates the need for life-long endocrine monitoring of PROP-1-deficient patients.

Adolescent↗
PubMed1973

[Pituitary hormones].

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Adrenocorticotropic Hormone↗
PubMed1981

Effects of a Met-enkephalin analogue and naloxone infusion on anterior pituitary hormone secretion in acromegaly.

The effect of a long-acting analogue of Met-enkephalin (Damme) and naloxone on anterior pituitary hormone secretion has been investigated in 14 acromegalic patients. Damme produced a progressive fall in circulating LH and cortisol and stimulated prolactin release in normoprolactinaemic patients. Naloxone infusion significantly stimulated gonadotrophin and cortisol secretion without modifying basal prolactin release both in normo-and hyperprolactinamic patients. GH levels remained unchanged during naloxone and Damme infusion. The data suggest that endogenous opiate receptors do not play a major role in modulating GH hypersecretion in acromegaly.

Acromegaly↗
PubMed1999

Targeted expression of toxic genes directed by pituitary hormone promoters: a potential strategy for adenovirus-mediated gene therapy of pituitary tumors.

Pituitary adenomas cause clinical manifestations because of mass effects and excess hormone production. This group of tumors represents a tractable target for gene therapy because they are rarely metastatic and because reductions in tumor size and function, in addition to those achieved after surgery, may be of clinical benefit. In this report we describe a strategy for targeting the expression of toxic genes to pituitary cells using adenoviral vectors. Pituitary hormone promoters (human GH or glycoprotein hormone alpha-subunit) were used to express either a marker gene [beta-galactosidase (beta-gal)] or a toxic gene [herpes simplex virus thymidine kinase (TK)]. In GH-producing GH3 cells and in alpha-subunit-producing pituitary tumor cell lines, recombinant adenoviruses containing either the alpha-subunit promoter (Ad alpha Gal; AdaTK) or the GH promoter (AdGHGal; AdGHTK) were expressed at-high levels. Using histological studies and assays for beta-gal activity, expression was shown to persist for at least 21 days, and it was relatively selective for pituitary cell lines. Cytotoxicity studies were performed using the TK-containing vectors and treatment with ganciclovir. Both AdGHTK and AdaTK caused greater than 95% cytotoxicity of GH3 and alphaT3 cells, respectively, at a viral dose (multiplicity of infection, 5 plaque-forming units/cell) that induced minimal toxicity using control viruses. Little cellular toxicity was seen using a nonpituitary cell line (T47D breast tumor cells). The AdGHTK virus also caused marked reduction in the size of GH3 cell tumors that were propagated in nude mice. These studies suggest that adenoviral vectors carrying human pituitary gland specific promoters may be useful for developing gene therapy strategies for the treatment of pituitary adenomas.

Adenoma↗
PubMed1978

Effects of intravenous isoxsuprine and ritodrine, with and without concomitant dexamethasone, on fetoplacental and pituitary hormones and cyclic adenosine monophosphate during late pregnancy.

Beta sympathomimetic drugs are used to inhibit preterm labor and glucocorticoids to accelerate fetal pulmonary maturation. A study was designed to investigate the hormonal effects of intravenous infusion of isoxsuprine 150 to 200 mcg. per minute or ritodrine 100 to 150 mcg. per minute in a series of 28 women at 28 to 40 weeks' gestation, with and without concomitant dexamethasone therapy. Serial serum samples taken before and during the six hours of infusion were assayed for cyclic adenosine-3,5-monophosphate (AMP), estradiol, estriol, progesterone, human placental lactogen (hPL), thyrotropin (TSH), follicle-stimulating hormone (FSH), and human growth hormone (gGH). Ritodrine was more potent than isoxsuprine in increasing the circulating levels of cyclic AMP. The levels of placental steroid hormones decreased slightly, as did the ratio of progesterone to estradiol. Human placental lactogen and pituitary hormones showed no consistent changes. Simultaneous administration of dexamethasone did not modify these results.

Adult↗
PubMed1978

Pituitary hormones and ergot alkaloids.

From the data presented it appears that ergot drugs are both a useful tool for use in the study of neuroendocrine control of pituitary hormone secretion and a valid pharmacologic weapon for treatment of hyperprolactinemic states, GH and, probably, ACTH and MSH hypersecretion. In fact, they are capable of a long-lasting disruption of PRL secretion from a normal or tumoral pituitary gland, are unable to affect directly the somatotrophs of an intact AP, but inhibit GH and, possibly, ACTH secretion from a hyperplastic or tumoral gland. Ergolines also exert clear-cut PRL-lowering effects and are capable of suppressing GH secretion in acromegaly. The intimate mechanism(s) and hence site(s) of action of some of these compounds await clarification.

Acromegaly↗