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Biomedical subjects

F Petraglia

Publications and source records attributed to F Petraglia.

At least 253 records · Page 14Linked to original sources
PubMed1990

Plasma beta-endorphin and beta-lipotropin levels increase in well trained athletes after competition and non competitive exercise.

Plasma beta-endorphin (beta-EP) and beta-lipotropin (beta-LPH) levels were measured in 15 healthy trained marathon runners. These hormones were evaluated in two different conditions: 1-before (1h) and after a marathon race (n = 10); 2-before, during and after a prolonged (90 min) submaximal exercise (bicycle ergometer at 50% VO2 max) (n = 5). In these latter group plasma beta-EP and beta-LPH levels were measured every 15 min for 165 min. In all the athletes, both plasma beta-EP and beta-LPH levels were significantly higher after the end of the marathon race than in basal conditions (p less than 0.01). The prolonged exercise with bicycle ergometer significantly stimulated plasma beta-EP and beta-LPH levels. Starting 60 min after the beginning of the exercise, plasma beta-EP and beta-LPH levels resulted significantly higher than basal values until the end of the exercise (p less than 0.01 at 60, 75 and 90 min). These data confirming that marathon running is a potent stress stimulus, showed that the duration and related factors but not the work load may be considered critical in stimulating beta-EP and beta-LPH release during physical exercise.

Adult↗
PubMed1990

Effect of steroid hormones and antihormones on hypothalamic beta-endorphin concentrations in intact and castrated female rats.

The aim of the present study was to evaluate the effects of estrogens and androgens on hypothalamic beta-endorphin (beta-EP) concentrations. Intact or castrated female rats were chronically (2 weeks) treated with estrogen (estradiol benzoate) and/or antiestrogens (clomiphene, cyclophenil or epimestrol), and with androgens (dihydrotestosterone or dehydroepiandrosterone sulphate) and/or antiandrogen (cyproterone acetate). A group of rats treated with vehicle were studied as comparison. The beta-EP concentrations were measured by radioimmunoassay on acidic extracts of rat hypothalami. The administration of clomiphene and cyclophenil significantly reduced hypothalamic beta-EP concentrations in intact rats, while both drugs or estradiol benzoate increased the peptide concentration in castrated rats. Both intact and castrated rats treated with epimestrol showed hypothalamic beta-EP concentrations higher than vehicle treated rats. The estradiol-induced increase of beta-EP was not changed by the concomitant administration of antiestrogens. The administration of dihydrotestosterone significantly decreased beta-EP concentrations in both intact and castrated female rats, while the treatment with dehydroepiandrosterone sulphate only slightly decreased beta-EP levels in intact female rats. The cyproterone acetate-chronically treated rats showed higher beta-EP concentrations than vehicle-treated rats and these changes were reversed by the concomitant addition of dihydrotestosterone or dehydroepiandrosterone sulphate. These results showed that estrogens play a positive role while androgens negatively influence the hypothalamic beta-EP concentrations in female rats, supporting the view that central beta-EP might be a target of gonadal steroid feedback signals.

Androgen Antagonists↗
PubMed1990

Relationship between cerebrospinal fluid beta-endorphin and plasma pituitary-gonadal hormone levels in women.

Brain beta-endorphin (beta-EP) plays an important role in regulating the hypothalamus-pituitary-gonadal axis activity. Cerebrospinal fluid (CSF) beta-EP levels seem to reflect the central rather than pituitary secretion. With the aim to correlate the changes of plasma estradiol (E2), progesterone, luteinizing hormone (LH) and follicle-stimulating hormone with brain beta-EP, CSF levels of beta-EP were measured in 15 normally cycling and 15 postmenopausal women. CSF beta-EP levels in post-menopausal women were lower than in fertile women. A positive correlation between plasma E2 and CSF beta-EP level was found in all women. In fertile women CSF beta-EP levels were inversely correlated to plasma gonadotropin levels. These results showed that CSF beta-EP levels differ between fertile and postmenopausal women and are correlated with plasma LH and E2, suggesting a strong linkage between central beta-EP levels and pituitary-gonadal axis hormones.

Adolescent↗
PubMed1990

Mechanism of action of interleukin-1 beta in increasing corticotropin-releasing factor and adrenocorticotropin hormone release from cultured human placental cells.

The present study evaluated the possible effect and mechanism of action of interleukin-1 beta in regulating the release of corticotropin-releasing factor and adrenocorticotropin hormone from human cultured placental cells. With the use of a primary monolayer culture of human placental cells at term, the addition of interleukin-1 beta increased the release of immunoreactive corticotropin-releasing factor with a dose- and time-dependent effect. The intracellular concentration of both cyclic adenosine monophosphate and cyclic guanosine monophosphate increased in the presence of interleukin-1 beta. The addition of indomethacin, a prostaglandin synthesis inhibitor, partially reversed the effect of interleukin-1 beta. The same doses of interleukin-1 beta stimulated the release of adrenocorticotropin hormone and this effect was partially reversed by the addition of a synthetic corticotropin-releasing factor antagonist or by indomethacin. This study showed that interleukin-1 beta increases the release of corticotropin-releasing factor and adrenocorticotropin hormone from cultured placental cells. This effect is associated with increased intracellular cyclic nucleotide concentrations and is in part reversed by a prostaglandin synthesis inhibitor.

Adrenocorticotropic Hormone↗
PubMed1990

Presence of ACTH and beta-endorphin immunoreactive molecules in the freshwater snail Planorbarius corneus (L.) (Gastropoda, Pulmonata) and their possible role in phagocytosis.

The presence of ACTH and beta-endorphin immunoreactive molecules in the cell-free hemolymph and in the hemocytes of the freshwater snail Planorbarius corneus were demonstrated by immunocytochemistry and RIA tests. Only spreading phagocytic hemocytes were positive, in contrast with other hemocytes devoid of phagocytic activity, i.e., round hemocytes. These data were confirmed by flow cytometry. Another cell type with marked phagocytic activity, i.e., digestive cells of digestive gland, were also positive to anti-ACTH. Corticotropin-releasing factor immunoreactive molecules were found in the cell-free hemolymph and hemocytes, by RIA. Our data suggest that cells with phagocytic activity, the oldest immune response, may represent a suitable model to unravel the tangled web of the common ancestor of the immune and the neuroendocrine systems.

Adrenocorticotropic Hormone↗
PubMed1990

Evidence of luteinizing hormone secretion in hypothalamic amenorrhea associated with weight loss.

The lack of plasma luteinizing hormone (LH) pulsatile pattern or episodic LH secretory bursts during night have been demonstrated in hypothalamic amenorrhea. The availability of both sensitive and specific immunofluorimetric assay and algorithm for pulse detection enabled us to reanalyze the question of whether or not patients with hypothalamic amenorrhea secrete LH in a pulsatile fashion. Seven women with secondary amenorrhea associated with weight loss and four normally cycling women were studied, sampling every 5 minutes for 8 hours. Control subjects were studied during four different phases of the menstrual cycle. In all amenorrheic patients, a frequent LH pulsatile secretion, with pulses of low amplitude, was found (10.7 +/- 1.4 peaks/8 h; mean +/- SEM). The pulse frequency was significantly higher (P less than 0.05) than any phases of the control group (early follicular: 7 +/- 0.4 peaks/8 h; late follicular: 6.8 +/- 0.6 peaks/8 h; early luteal: 4.3 +/- 0.4 peaks/8 h; late luteal: 7 +/- 0.3 peaks/8 h). The LH pulsatile release in amenorrheic patients showed a mean pulse duration and amplitude shorter than in any phase of the menstrual cycle of the controls. In conclusion, in weight-loss-related-amenorrhea, the major change was not the absence of the LH pulsatile release but its increased frequency with reduced pulse amplitude.

Adolescent↗
PubMed1990

Pregnancy following combined growth hormone--pulsatile GnRH treatment in a patient with hypothalamic amenorrhoea.

A patient with hypothalamic amenorrhoea and a poor response in terms of pituitary growth hormone (GH) to acute administration of growth hormone-releasing factor has been treated with pulsatile gonadotrophin-releasing hormone (GnRH) combined with GH to induce ovulation. GH was administered daily until signs of ovulation were detected. The luteal phase was supported by pulsatile GnRH only. Combined treatment gave an improved follicular recruitment, higher plasma levels of 17 beta-oestradiol and an earlier ovulation, compared to the previous cycle with pulsatile GnRH only. The result was a twin pregnancy which ended with the birth of two healthy male babies. The role of GH in potentiating the ovarian response to gonadotrophins, as well as the GH secretion abnormalities associated with dysfunctions of the hypothalamic - pituitary - gonadal axis, might provide a rationale for combined GH and pulsatile GnRH treatment in such patients.

Adult↗
PubMed1990

Estimation of instantaneous secretory rate of luteinizing hormone in women during the menstrual cycle and in men.

In both men and women the pulsatile secretory pattern of LH has been extensively characterized. In the present study we used the algorithm for computation of instantaneous secretory rate (ISR) incorporated into the DETECT program to evaluate the secretory activity of gonadotrophs in vivo. We studied the pulsatile release of LH in four healthy women during four phases of the same menstrual cycle (early and late follicular and luteal phases) and in five healthy men. Computation of ISR permitted us to estimate the frequency and the duration of the secretory events from the gonadotrophs. Samples were collected every 10 min for 6 h. The apparent LH pulsatile frequency during the menstrual cycle varied from 5.0 +/- 0.8 (mean +/- SD) during the early follicular phase (EFP) to 5.3 +/- 1.2 peaks/6h during the late follicular phase (LFP), to 3.3 +/- 1.0 during early luteal phase (ELP) and to 5.3 +/- 0.4 peaks/6h during the late luteal phase (LLP). The mean pulse duration also changed throughout the phases of the cycle (EFP 47.4 +/- 13.2 min; LFP 55.4 +/- 21.6 min; ELP 100 +/- 50.4 min; LLP 48.1 +/- 11 min). In healthy men the LH pulse frequency was 3.8 +/- 1.6 peaks/6h and the duration was 71.5 +/- 35.7 min. When time series were analysed for ISR determination no significant changes were observed between the LH pulse frequency detected on ISR and that observed on plasma concentrations. Conversely, a significant reduction of the duration of the pulses was found when using ISR instead of plasma concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Dementia of the Alzheimer type and hypothalamus-pituitary-adrenocortical axis: changes in cerebrospinal fluid corticotropin releasing factor and plasma cortisol levels.

The activity of the hypothalamus-pituitary-adrenocortical (HPA) axis was explored in 10 patients with dementia of the Alzheimer type (DAT) and in 11 age-matched controls, by measuring 1) corticotropin-releasing factor (CRF) levels in cerebrospinal fluid (CSF), 2) the circadian changes of plasma cortisol, 3) and 4) the plasma cortisol response to dexamethasone suppression test (DST) and to CRF stimulation test. CSF CRF levels in DAT were significantly higher than in controls and inversely related to the Mini Mental State (MMS) score. The patients also displayed increased morning (0800 h) plasma cortisol values, with higher mesor and amplitude in the circadian pattern. Dexamethasone resistance was shown by 6 of the 10 DAT subjects. Plasma cortisol response to CRF administration was similar in the two groups, except for the peak values, which in DAT patients were reached earlier than in controls. The present data suggest an overactivity of HPA axis in DAT; its possible role in the evolution of the disease is discussed.

Aged↗
PubMed1990

Estrogens modulate the circadian rhythm of hypothalamic beta-endorphin contents in female rats.

The aim of the present study was to evaluate the changes in the diurnal rhythm of the hypothalamic beta-endorphin (beta-EP) contents in female rats as a function of circulating estrogens. With this purpose we evaluated the diurnal hypothalamic beta-EP changes (1) during the estrous cycle, and (2) in ovariectomized rats with and without acute and chronic estrogen replacement. Ovariectomized rats were treated either acutely with 10 micrograms of estradiol benzoate (EB) or chronically with 2 micrograms/day of EB for 15 days. beta-EP concentrations were measured in acid extracts of medial basal hypothalamus by a specific radioimmunoassay. During the estrous cycle, hypothalamic beta-EP concentrations showed a significant nocturnal increase, with no difference between the 4 days of the cycle. On the day of estrus, beta-EP concentrations between 12.00 and 18.00 h resulted significantly lower than in the other days of the cycle. After ovariectomy, the night-related changes in hypothalamic beta-EP disappeared. The acute administration of EB induced a significant increase in hypothalamic beta-EP after 21 h (18.00 h). On the other hand, the chronic replacement restored the nocturnal peak of hypothalamic beta-EP (18.00, 21.00, 24.00 h). The present data emphasize the role of central beta-EP in regulating the reproductive functions. Moreover, the effect of estrogen in modulating the circadian changes in hypothalamic beta-EP supports the important role of estrogens in brain function.

Animals↗
PubMed1990

Progestins modulate the action of estrogen on gonadotropin-releasing hormone, luteinizing hormone and prolactin in the rat.

The aim of the present study was to evaluate the effect of progesterone and of various synthetic progestins on hypothalamic gonadotropin-releasing hormone (GnRH) and on pituitary and plasma LH and prolactin (Prl) concentrations in ovariectomized rats. Groups of 6 rats were treated for 2 weeks with a pharmacological dose of progesterone, desogestrel, medroxyprogesterone acetate or norethisterone enanthate (NET). The same treatment was also repeated in association with estradiol benzoate (EB). Groups of ovariectomized rats were also treated with EB only or vehicle. Ovariectomized rats showed hypothalamic concentrations of GnRH significantly higher than control rats. Progesterone and NET significantly increased GnRH concentrations and reversed the EB-induced changes. Rats treated with progesterone and NET also showed reduced pituitary LH concentration, with high plasma LH levels. All progestins blocked the increase of pituitary LH induced by EB, but were inactive in influencing the inhibitory effect of EB on plasma LH levels. The administration of progesterone and progestins did not induce significant changes of pituitary or plasma Prl, but reversed the EB-induced increase. These results showed that progesterone and progestins have a marked effect on hypothalamic and pituitary hormone secretion and that they modulate estrogen-induced effects.

Animals↗
PubMed1990

Steroid hormones modulate the release of immunoreactive gonadotropin-releasing hormone from cultured human placental cells.

The aim of the present study was to evaluate whether steroid hormones or opiate receptor agonists participate in the mechanisms regulating the release of immunoreactive GnRH (irGnRH) from cultured human placental cells. No significant changes in irGnRH concentrations were found in the culture medium after 48-h incubation of estradiol, estriol, or progesterone. Both estriol and estradiol augmented, while progesterone decreased, the irGnRH release induced by 8-bromo-cAMP. The stimulatory effect of estriol or estradiol was reversed by the concomitant addition of progesterone. The secretagogue effect of activin on irGnRH release from cultured placental cells was increased by the presence of estriol and reduced by the addition of progesterone. The action of estriol was counteracted by both tamoxifen, an estrogen antagonist, and progesterone. The inhibitory effect of progesterone was completely reversed by RU 486, a specific receptor antagonist. The addition of morphine, methionine-enkephalin, or UP50, 488H which preferentially bind mu-, delta-, and kappa-opiate receptors, respectively, did not decrease basal irGnRH release from cultured human placental cells. However, both morphine and UP50, 488H significantly inhibited 8-bromo-cAMP-induced GnRH release. The present results showed that steroid hormones and opiate receptor agonists influence irGnRH release from human cultured cells, suggesting that local interaction between steroids and peptides modulates irGnRH release from human placenta.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1990

Presence and synthesis of inhibin subunits in human decidua.

A growing number of studies provided the evidence that human decidua is a pregnancy-related tissue capable of hormone production and metabolism. The aim of the present study was to evaluate the possible presence of inhibin subunits in human decidua. Tissue samples were collected in pregnant women during the first (8 weeks) and second trimester (18 weeks) of gestation and at term (40 weeks). Immunohistochemical data were obtained using affinity purified polyclonal antisera raised in rabbit against porcine alpha, beta A, or beta B subunits. Levels of the respective inhibin subunits were evaluated by Northern blot analysis using cDNA probes encoding sequences corresponding to each subunit. The present results indicated that human decidua contains and synthesizes inhibin alpha, beta A, and beta B subunits. The immunohistochemical data showed that decidual cells were stained with both inhibin alpha and beta B antisera, showing a similar localization. On the other hand, cells stained with inhibin beta A antisera were sparse and followed a distribution pattern different from that of cells stained with alpha or beta B antisera. The first inhibin alpha and beta B subunit mRNAs were both expressed in first trimester of pregnancy, and those mRNA levels showed a gestational related increase. The beta A subunit mRNA was expressed at very low levels at term and could not be detected earlier during pregnancy. The present data showed that human decidua actively produces inhibin subunits with a gestational-related profile. The results suggest that decidua may be a further source of inhibin-related proteins during pregnancy and emphasize the endocrine competence of human decidua.

Abortion, Spontaneous↗
PubMed1990

Changes in beta-endorphin in fetal membranes and placenta in normal and pathological pregnancies.

Several studies indicated that trophoblast tissue synthesizes pro-opiomelanocortin-related peptides. These peptides are also present in amniotic fluid, but their origin remains unknown. The present study evaluated the presence of and the possible changes in beta-endorphin (beta-EP) in amnion and chorion during pregnancy, at parturition and in spontaneous abortion. Amnion, chorion and placental tissues were isolated and homogenized from a total of 46 pregnant women between 4th and 42 th week of pregnancy. Beta-EP was separated on a Sephadex G-75 column and measured by RIA with specific antiserum. The identity of the endogenous opioid with its corresponding reference molecule was confirmed by high performance liquid chromatography. In all tissues, the concentration of beta-EP in the first trimester was significantly higher than in the second trimester. A negative correlation between opioid levels and gestational age was observed in the first two trimesters. At delivery, the beta-EP content of all tissues was greater than in the second trimester. In tissues collected at term, in the absence of labor, beta-EP levels were very low in comparison with those collected after vaginal delivery. Low beta-EP contents were found in membranes collected from spontaneous abortion in 1st trimester. From these data one can surmise the existence of a local endogenous opioid system in fetal adnexes. This system seems sensitive to the stress of vaginal delivery and could be involved in the mechanisms leading to spontaneous abortion.

Abortion, Spontaneous↗
PubMed1990

Corticotropin-releasing factor and parturition: plasma and amniotic fluid levels and placental binding sites.

We evaluated levels of corticotropin-releasing factor in the plasma and amniotic fluid of women who had spontaneous vaginal delivery or elective cesarean. Corticotropin-releasing factor binding sites were also studied in placental tissue collected from vaginal or cesarean birth. Plasma samples were collected hourly from seven women from the onset of labor until delivery, and from ten women before and during elective cesarean. Amniotic fluid samples were collected from 40 women at different stages of labor and from ten women during elective cesarean. Maternal plasma corticotropin-releasing factor levels increased during labor, showing the highest values at delivery. No significant differences in amniotic fluid immunoreactive corticotropin-releasing factor levels were observed at the different stages of cervical dilatation. At cesarean, maternal plasma levels did not differ significantly from those found before surgery, and in the amniotic fluid they were similar to those found in pregnancy. The number of 125I-corticotropin-releasing factor binding sites in placental tissue was higher after vaginal than after cesarean delivery. These results suggest that corticotropin-releasing factor secretion is activated by the stress of labor.

Adult↗
PubMed1989

Neurotransmitters and peptides modulate the release of immunoreactive corticotropin-releasing factor from cultured human placental cells.

The substances stimulating the release of immunoreactive corticotropin-releasing factor from cultured human placental cells were investigated. Monolayer primary cultures of trophoblast cells from pregnant women at term were used. The immunoreactive corticotropin-releasing factor released in the culture medium eluted from high-performance liquid chromatography with the same retention time as human corticotropin-releasing factor. Norepinephrine and acetylcholine increased immunoreactive corticotropin-releasing factor release into the culture medium in a dose-related manner. Epinephrine was partially active, whereas dopamine and serotonin did not induce significant changes of immunoreactive corticotropin-releasing factor release from placental cultures. Angiotensin II, interleukin-1, oxytocin, and arginine-vasopressin also increased placental immunoreactive corticotropin-releasing factor release in a dose-related manner, whereas other peptides (vasoactive intestinal peptide, substance P, somatostatin, atrial natriuretic factor, interleukin-2) were ineffective. These results showed that several neurotransmitters and peptides stimulate the release of immunoreactive corticotropin-releasing factor from placental cells, suggesting their possible involvement in the physiologic regulation of placental immunoreactive corticotropin-releasing factor release during pregnancy and parturition.

Acetylcholine↗
PubMed1989

Norgestimate increases pituitary and hypothalamic concentrations of immunoreactive beta-endorphin.

Progesterone is a potent hormone acting on the female reproductive tract and influencing a series of other functions. Recent studies revealed a correlation between progesterone and brain neurotransmitters and neuropeptides. Our study evaluated the possible effect of norgestimate, a new progestin, on hypothalamic and pituitary beta-endorphin (B-EP) concentration in castrated female rats. Ovariectomy was performed under ethyl ether anesthesia. Treatment was started 3 weeks after surgery. Norgestimate, estradiol benzoate or norgestimate plus estradiol benzoate were administered. The two steroids were dissolved in sesame oil and injected (s.c.) every day for 2 weeks. Pituitary and hypothalamus B-EP concentrations were measured by radioimmunoassay. Our studies showed that norgestimate increases the pituitary and hypothalamic B-EP concentration in female rats, reaching values higher than controls and estrogen-treated rats. Because B-EP has an important role in reproductive function, both modulating gonadotropin secretion and sexual behavior, the present results lead to the hypothesis that norgestimate affecting B-EP concentrations may influence central functions.

Animals↗