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PubMedDate not supplied

Effects of neuropeptide Y (NPY) on the release of anterior pituitary hormones in the rat.

Neuropeptide Y (NPY) has been recently localized in several hypothalamic nuclei in the mammalian brain. In order to investigate the possible role of NPY on neuroendocrine function, we have investigated the effects of the peptide on the release of anterior pituitary hormones in the rat. Both intravenous (300 micrograms) or intraventricular (2 to 15 micrograms) injection of NPY produced in gonadectomized male rats a significant and long-lasting decrease of plasma LH levels. A short duration stimulating effect on prolactin plasma levels was also observed after the intravenous but not after the intraventricular injection of NPY. Plasma levels of the other pituitary hormones were not significantly modified after NPY injection. When incubated in vitro with anterior pituitary cells in monolayer culture, NPY produced no significant change in release of pituitary hormones. Thus NPY seems to exert a selective effect on LH release. Since this effect can be observed after both intravenous and intraventricular injection, it might be hypothesized that NPY could affect LHRH release in two areas which lack blood-brain barrier: the organum vasculosum of the lamina terminalis (OVLT) which contains LHRH cell bodies and NPY fibers and the median eminence which contains both LHRH and NPY fibers. The effect on prolactin release needs to be carefully evaluated in different experimental conditions.

Animals↗
PubMedDate not supplied

[Neuropharmacological regulation of pituitary hormones. Role of acetylcholine, gamma-aminobutyric acid, histamine and endorphins (author's transl)].

The secretion of pituitary hormones is controlled by hypothalamic hormones which are synthetized by neurosecreting cells whose activity is modulated by different neurotransmitters as dopamine and serotonin. Centrally acting drugs interfere with the activity of these neurotransmitters. Thus they may influence the secretion of pituitary hormones. Acetylcholine, gamma-aminobutyric acid, histamine and endorphins seem also to influence the pituitary secretion. The endocrine effects of drugs (opiates, antiparkinson, antiepileptic, and antihistaminic agents) acting on these neurotransmitters is reviewed.

Acetylcholine↗
PubMed1997

[Paracrine regulation of anterior pituitary hormones by neuropeptides].

The hypothalamus is the source of neuropeptides which, being secreted into the portal system, control the synthesis and the secretion of the anterior pituitary hormones. Besides the well characterized hypothalamic central control and the hormonal peripheral control, recent studies have shown, in the anterior pituitary, the expression, among many other regulatory factors, of neuropeptides that are identical to those produced by the hypothalamus and that seem involved in the local control of anterior pituitary functions through autocrine or paracrine mechanisms. The presence of the neuropeptide mRNAs, precursors and mature forms of the peptides in anterior pituitary tissues as well as the secretion of the mature peptides argue in favor of the intrinsic ability of the normal and tumoral anterior pituitary to express neuropeptides. This expression of neuropeptides occurring in tissues bearing functional receptors for these ligands, anterior pituitary control could rely, at least in part, on endogenous neuropeptides acting locally. Correlations between neuropeptide contents in the anterior pituitary and the plasma levels of anterior pituitary hormones suggest that neuropeptides of anterior pituitary origin can play a local regulatory role, complementary of the classical hypothalamic central control. In the normal anterior pituitary which remains under hypothalamic control, it is presently difficult to evaluate the relative importance of the local and central control. However, anterior pituitary hyperplasia and pituitary tumors represent two models in which the specific contribution of the local control is easier to define.

Animals↗
PubMed1975

The response of pancreatic and pituitary hormones to pulses and constant infusion of somatostatin.

The inhibitory action of pulses and constant infusion of somatostatin on the secretion of pancreatic and pituitary hormones was studied serially in 7 normal men and 2 untreated acromegalics. In normal men, significant inhibition of basal release of insulin and glucagon was elicited by as little as 1 mug dose of a pulse of somatostatin. Increasing doses of somatostatin (5, 50, 250 and 500 mug) given as a single pulse at weekly intervals produced what appears to be a decreased inhibition of glucagon while no measurable relationship between the dose of somatostatin and the degree of inhibition of insulin was seen. Given during the same day, incremental doses (from 1 to 250 mug) of pulses of somatostain produced a progressive decline in both glucagon and insulin. The elevated basal levels of GH, insulin and glucagon seen in acromegalics, were inhibited by a pulse of somatostatin as little as 2 mug. These inhibitions were sustained during the constant infusion of somatostatin (2.5 mug/min), and a rebound in GH, insulin and glucagon appeared promptly following the infusion.

Acromegaly↗
PubMed2004

Chromosomal translocation t(10;11)(q26;q13) in a woman with combined pituitary hormone deficiency.

We describe the case of a girl with combined pituitary hormone deficiency (CPHD) carrying a balanced chromosomal translocation t(10;11)(q26;q13) with paternal transmission. Her father, with no apparent physical abnormalities, had the karyotype: 46, XY, t(10;11)(q26;q13). CPHD denotes impaired production of growth hormone (GH) and one or more of the other five anterior pituitary-derived hormones. Pit-1 gene and Prop-1 gene mutations and deletions have been reported being responsible for CPHD. Although our patient had a t(10;11) (q26q13) paternal chromosomal translocation, the phenotype was similar to that found in humans with different Pit-1 or Prop-1 gene alterations. Interestingly, the patient's father had the same translocation without phenotypic effects. In conclusion, we describe panhypopituitarism in a woman with a paternally transmitted translation, which appears to be phenotypically expressed only in females.

Adult↗
PubMed1988

Effects of daytime noise load on the sleep-wake cycle and endocrine patterns in man: II. 24 hours secretion of anterior and posterior pituitary hormones and of cortisol.

The present study examines the effects of auditory stress on the plasma levels of pituitary hormones and cortisol. Each of twelve healthy male subjects participated in two experimental series; during one of them they were exposed to 85 dB(A) industrial noise from 9:00 to 21:00 h. Blood samples were taken by an indwelling venous catheter for 24 h at intervals of 20 min from 8:00 to 8:00 h. The plasma levels of ACTH, growth hormone, prolactin, oxytocin, vasopressin and cortisol were determined. In all subjects except one noise stress affected the profiles of the pituitary hormones but the responses were interindividually different. The oxytocin level was significantly elevated (p less than .01), ACTH also responded but less clearly, whereas the other hormones reacted only in individual cases. During the subsequent night sleep only PRL concentrations were elevated above the baseline plateau in several subjects. It was concluded that in humans the pituitary responses to noise stress are highly individual.

Adult↗
PubMed1984

Recent studies on the role of brain peptides in control of anterior pituitary hormone secretion.

Recent work in our laboratory on the role of peptides to influence release of pituitary hormones by direct action on the gland and also some of the interactions of these peptides at the hypothalamic level to alter release of pituitary hormones will be reviewed. Considerable evidence from hypothalamic stimulation and lesion studies suggests the existence of a separate FSH-releasing factor (FSHRF). We have been able to purify a bioactive FSHRF which appears to be distinct from LHRH. Consequently, we believe that a distinct FSHRF will ultimately be isolated. With regard to prolactin, it is now clear that it is under dual control by both prolactin-inhibiting (PI) and prolactin-releasing factors (PRF). Although dopamine acts as a PIF, our recent fractionation studies indicate the existence of a peptidic PIF in hypothalamic extracts which can be separated from dopamine and GABA. The peptidic PIF is eluted from Sephadex in the same position originally described by us a number of years ago. Thus, inhibitory control is probably mediated by a combination of factors which would include dopamine, possibly GABA and a peptidic PIF. A number of peptides have been shown to have PRF activity which include TRF and also VIP. In recent studies, we have shown a prolactin-releasing action of oxytocin on male hemipituitaries or dispersed pituitary cells. Furthermore, high doses of oxytocin given intravenously released prolactin in male rats. There is a correlation between estrogen-induced prolactin release and an increase in plasma oxytocin and a correlation between suckling-induced oxytocin and prolactin release. These results suggest that oxytocin may be an important PRF.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

The molecular pathology of pituitary hormone deficiency and resistance.

In this chapter, we have reviewed the fast-moving area of the molecular pathology of pituitary hormone deficiencies and resistance. Examples have been described affecting all levels of pituitary function, i.e. the releasing hormone, its receptor, the pituitary hormone and its receptor, and the development of the pituitary gland. Other examples in these genes, and in those in which no mutation has yet been found, will undoubtedly be discovered in the next few years, throwing light on the structural basis of the gene product's function and allowing a greater understanding of endocrine physiology and pathophysiology. The main reason for this rapid progress in knowledge is the recent technological advances in mutation detection, which bring this activity within the grasp of the majority of reasonably equipped laboratories. Technological advancement, however is not all that it takes to carry out this work. The conditions caused by genetic damage such as we have described are rare, and there is clearly a requirement for great awareness on the part of the clinical endocrinologist. Patients in whom it is suspected that mutations such as these may occur require careful clinical and biochemical work-up. Indeed, in many instances, careful thought has to go into deciding what the phenotype of a particular mutation might be. Thus, the requirement for close collaboration between clinical and molecular endocrinologists has to be the important message for the future in this area of research.

Adrenocorticotropic Hormone↗
PubMed2001

Effects of exogenous melatonin on pituitary hormones in humans.

The effects of melatonin on physiological function remain unclear, although the therapeutic potential of melatonin is being increasingly recognized. The aim of the present study is to investigate the effects of exogenous melatonin on the spontaneous release of pituitary hormone in humans. A double blind placebo-controlled protocol was designed to examine 12 adult healthy volunteers and 12 sleep disorder patients who have been treating with low doses of melatonin for 1 year. Either exogenous melatonin or placebo of 1 mg was given at 09:00 hours, followed by the collection of blood samples every 20 min for 4 h. Each blood sample was examined for levels of serum melatonin, PRL, LH, FSH, GH and TSH. LH levels were higher in sleep disorder patients compared with the healthy volunteers. In other pituitary hormones, there were no significant difference between healthy adults and sleep disorder patients. In all subjects, PRL levels were stimulated by acute administration of 1 mg of exogenous melatonin, while the levels of other pituitary hormones were not affected. These results suggested that exogenous melatonin can affect the spontaneous release of LH and PRL in humans. In addition, we demonstrated that 1-year oral melatonin treatment did not affect the responses to the acute administration of melatonin.

Administration, Oral↗
PubMed1999

Electron Microscopic and Confocal Laser Scanning Microscopic Observation of Subcellular Organelles and Pituitary Hormone mRNA: Application of Ultrastructural In Situ Hybridization and Immunohistochemistry to the Pathophysiological Studies of Pituitary Cells.

Nonradioisotopic electron microscopic (EM) in situ hybridization (ISH) (EM-SH) with biotinylated oligonucleotide probes is utilized for the ultrastructural visualization of pituitary hormone mRNA in rat pituitary cells. EMISH is an important tool for clarifying the intracellular localization of mRNA and the exact site of specific hormone synthesis on the rough endoplasmic reticulum. The simultaneous visualization of mRNA and encoded protein in the same cell using preembedding EM-ISH and subsequent postembedding immunoreaction with protein A colloidal gold complex can provide an important clue for elucidating the intracellular correlation of mRNA translation and secretion of translated protein. Another focus of this review is the utilization of a recently developed imaging system of confocal laser scanning microscopy (CLSM). The combination of CLSM and image analysis system (lAS) enables us to visualize an individual dimensional image of the intracellular distribution of mRNA and subcellular organelles successfully at any optional cross sections of light microscopic ISH studies, and can be another useful tool for the ultrastructural ISH study of mRNA.

Journal Article↗
PubMed1987

The effects of the systemic administration of N-methylmorphine chloride, a quaternary analogue of morphine that does not cross the blood-brain barrier, on the release of anterior pituitary hormones in the rat.

The acute administration of morphine elicits changes in the release of anterior pituitary hormones. The locus of this action is thought to be in the central nervous system, specifically the hypothalamus. There are some data suggesting that systemically administered opiates and opioid peptides can act outside of the blood-brain barrier to influence anterior pituitary hormone release. To test this hypothesis we examined the effects of the systemic administration of N-methylmorphine chloride, a quaternary analogue of morphine that does not cross the blood-brain barrier, on the release of corticosterone, growth hormone, prolactin, luteinizing hormone, and thyroid stimulating hormone in the rat. N-methylmorphine caused increases in the release of growth hormone and prolactin, but serum levels of corticosterone, luteinizing hormone and thyroid stimulating hormone were unaffected. These results indicate that the opiate-induced release of growth hormone and prolactin may be mediated in part by sites outside of the blood-brain barrier.

Adrenocorticotropic Hormone↗
PubMed1991

Evaluation of the sites of opioid influence on anterior pituitary hormone secretion using a quaternary opiate antagonist.

Studies were conducted to determine the effects of a potent narcotic antagonist, nalmefene methyliodide, which does not cross the blood-brain barrier (BBB), on the secretion of anterior pituitary hormones and on the anterior pituitary hormonal response to morphine sulfate. Since the localization of opiate receptor responses to inside or outside the BBB depended upon the relative ability of nalmefene HCl and nalmefene methyliodide to penetrate the BBB, initial studies were conducted to document that nalmefene methyliodide does not block opiate receptors inside the central nervous system. While nalmefene HCl blocked morphine-induced antinociceptive responses at doses as low as 10 micrograms/kg, nalmefene methyliodide was ineffective in this regard at doses as high as 500 micrograms/kg. The luteinizing hormone (LH) suppression and prolactin (PRL) secretion induced by morphine was blocked by both nalmefene HCl and its methyliodide analogue, indicating that the opioid receptor type which mediates both responses is located outside the BBB. We observed that basal PRL levels were reduced by nalmefene HCl but not by nalmefene methyliodide indicating that basal PRL secretion is influenced by opioid neurons inside the BBB. While nalmefene HCl blocked morphine-induced suppression of thyroid-stimulating hormone (TSH) release, nalmefene methyliodide was less effective, suggesting that opiate-induced TSH suppression may be mediated by receptors located both within and outside the BBB. Nalmefene HCl caused a growth hormone (GH)-secretory response by itself, but nalmefene HCl and nalmefene methyliodide were ineffective in blocking morphine-induced GH secretion.(ABSTRACT TRUNCATED AT 250 WORDS)

Analgesia↗
PubMed1994

Application of biotinylated oligonucleotide probes to the detection of pituitary hormone mRNA using northern blot analysis, in situ hybridization at the light- and electron-microscope levels.

There have been many reports on radioisotopic in situ hybridization (ISH) studies for the demonstration of pituitary hormone mRNAs in normal pituitary gland and pituitary adenomas. Recent studies have revealed that non-radioisotopic ISH has several advantages over the radioisotopic method. Using ISH with biotinylated oligonucleotide probes, we have been able to localize various pituitary hormone mRNAs in paraffin wax or frozen sections of rat normal pituitary gland and human pituitary adenomas. For control studies we used ISH with sense probes, ISH without probes, pretreatment with ribonuclease, ISH with a probe for beta-actin and Northern blot hybridization. Using biotinylated probes, gene transcripts of rat growth hormone and prolactin were detected by Northern blot hybridization. The same biotinylated probes were used not for light microscope ISH but also for the electron microscopical demonstration of rat growth hormone and prolactin mRNAs on the polysomes of the rough endoplasmic reticula. It is emphasized that biotinylated oligonucleotide probes are useful for the analysis of pituitary endocrine function because they are applicable to the three hybridization methods, namely, Northern blot hybridization and ISH at the light and electron microscope levels.

Adenoma↗