Alessandro Mongioi

Involvement of Corticotropin-Releasing Hormone and Endogenous Opioid Peptides in Prolactin-Suppressed Gonadotropin Releasing Hormone Release in vitro

Corticotropin-releasing hormone (CRH) has been shown capable of inhibiting hypothalamic gonadotropin-releasing hormone (GnRH) release through activation of an endogenous opioid peptide (EOP)-dependent mechanism. Recently, we have shown that prolactin (PRL) stimulates CRH release and inhibits GnRH release by hypothalami explanted from male rats. Thus, the present study was undertaken to investigate whether the inhibitory effect of PRL on GnRH release in vitro is mediated by CRH and/or EOP. To this aim, the release of GnRH in response to PRL was evaluated in presence of CRH9-41 alpha-helical (CRH-9-41), a CRH receptor antagonist, and/or naloxone (NAL), a nonselective opioid receptor antagonist, using a static hypothalamic organ culture system which enabled us to evaluate immunoreactive GnRH (iGnRH) release from individually incubated longitudinally halved hypothalamic. As previously shown, PRL at the concentration of 100 nmol/l inhibited basal iGnRH release by about 35%. CRH9-41 or NAL overcame the inhibitory effect of PRL on iGnRH release in a concentration-dependent fashion. The simultaneous co-incubation with both antagonists was not more effective than each single antagonist. CRH9-41 did not have any effect on basal iGnRH release whereas NAL, as previously reported, increased it. In addition, PRL at the concentration of 100 nmol/l stimulated basal hypothalamic beta-endorphin (beta-EP) release. In conclusion, these data show that antagonism to CRH receptors counteracts the suppressive effects of PRL upon GnRH release and that PRL is able to stimulate hypothalamic beta-EP release in vitro.

Enhancing Detection of Gonococcus in Ejaculates of Adult Males Using Sperm Dilution

Specific cultures were used to detect growth of Neisseria Gonorrhoeae (NG) in 90 ejaculates of partners of childless marriages. Although no gonococcal growth was observed in undiluted semen, 9 out of 68 subjects with silent infection presented growth of NG in seminal plasma after dilution 1:2 with saline. It is concluded that semen dilution increases the chances of detection of NG in semen samples of asymptomatic gonococci carriers.

Pituitary and adrenal response to ovine corticotropin-releasing hormone in women with polycystic ovarian syndrome

It has been hypothesized that there is an adrenal abnormality in the polycystic ovary syndrome (PCO). This study was undertaken to examine this hypothesis in a more physiological way, by enhancing the ACTH secretion in response to ovine corticotropin releasing hormone (oCRH) injection so that adrenal androgen and glucocorticoid responsiveness to endogenous stimulation could be examined. Plasma ACTH and the ACTH and Cortisol (F) response to oCRH were normal. The plasma T and dehydroepiandrosterone (DHEA) responses were also normal. The androstenedione (A) response, however, was exaggerated. This study supports the hypothesis that the adrenal gland in patients with PCO produces increased amounts of androstenedione in response to ACTH stimulation.

lntra- and Inter-Individual Variability in Growth Hormone Responses to Growth Hormone-Releasing Hormone*.

Normal subjects show a wide range of growth hormone (GH) responses to growth hormone‐releasing hormone (GHRH) stimulation, but it is uncertain whether this variability reflects differences among individuals or whether it would also be observed on repeated tests of the same subject. To clarify this, we tested nine normal men repeatedly with iv bolus doses of 1 μg/kg GHRH(1–44)NH2. Most subjects showed wide variations in their GH responses on repeated testing, and the intra‐individual variability was nearly as great as the inter‐individual variability in responses, accounting for about two‐thirds of the overall variance. A minority of subjects had lower and less variable responses. Ultradian fluctuations in hypothalamic somatostatin secretion may account for this marked intra‐individual variability.

HYDROTESTOLACTONE LOWERS SERUM OESTRADIOL AND PRL LEVELS IN NORMAL MEN: EVIDENCE OF A ROLE OF OESTRADIOL IN PRL SECRETION*

The effect on serum PRL levels of lowering serum oestradiol (E2) concentration by short‐term administration of an aromatase activity inhibitor, hydrotestolactone (HT), was studied in six healthy male subjects. After HT administration serum E2 levels decreased from 68 ± 5±8 to 26 ± 2±5 pmol/1 (mean ± SE, P < 0±05). These E2 changes were accompanied by a significant decrease in mean 2‐h PRL levels from 11±2 ± 2±1 to 6±5 ± 1±6 ng/ml mean ± SE, P < 0±05). The evaluation of individual percentage change from basal concentrations showed a varying decrease in all subjects. These findings suggest that under physiological conditions E2 may be one of the factors which control blood PRL concentrations in men.

Some Critical Considerations on the Use of the Nomifensine Test in the Hyperprolactinaemic Syndrome

Nomifensine has recently been proposed as a dynamic test to discriminate tumoral from functional hyperprolactinaemia. In the present study, this test was performed in 9 subjects with radiological signs of sellar alteration and in 6 with no signs of pituitary lesion. Adopting the criterion reported in the previous study, the test was considered positive in 2 subjects of the first group and in 2 subjects of the second group. Therefore, our study indicates that the ability of this test to discriminate subjects with tumorous or non-tumorous hyperprolactinaemia still appears debatable.

Kinetics of steroid responsiveness to hCG during chronic inhibition of testicular function by GnRH analogue

The effect of daily injections of D-Ser-(TBU)6-LRH-EA10 (GnRH analogue (GnRH-A) 100 micrograms sc) on serum testosterone (T), 17 alpha-hydroxyprogesterone (17OHP) and oestradiol-17 beta (E2) was studied in 4 men. During GnRH-A therapy T, 17OHP and E2 were markedly decreased by the end of the second month. Continuous long-term administration of GnRh-A inhibited testicular function. To test whether the biosynthetic pathway was affected by the regimen, a bolus of 2000 U hCG was given to each subject after 10 months of therapy. Evaluation of the kinetics of steroid responsiveness showed a significant release of T in response to the trophic stimulus, with little or no elevation of serum 17OHP and E2. The response seen in these treated men appeared similar to that found in hypogonadotrophic men and prepubertal boys.