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P Chiodera, R Volpi, S Pilla, S Cataldo and V Coiro

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V Coiro, R Volpi, ML Maffei, A Caiazza, G Caffarri, L Capretti, R Colla and P Chiodera

Coiro V, Volpi R, Maffei ML, Caiazza A, Caffarri G, Capretti L, Colla R, Chiodera P. Opioid modulation of the gamma-aminobutyric acid-controlled inhibition of exercise-stimulated growth hormone and prolactin secretion in normal men. Eur J Endocrinol 1994;131:50–5. ISSN 0804–4643

The possible involvement of endogenous opioids in the gamma-aminobutyric acid-controlled (GABAergic) inhibition of growth hormone (GH) and prolactin (PRL) during physical exercise was evaluated in normal men. After fasting overnight, seven subjects were tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3-min intervals until exhaustion and lasted about 15 min in all subjects. Tests were carried out under administration of placebo, the opioid antagonist naloxone (10 mg as an iv bolus injection), the GABAergic agonist sodium valproate (600 mg in three divided doses orally) or naloxone plus sodium valproate. During exercise, plasma GH and PRL levels rose 5.5- and 1.9-fold, respectively. The administration of naloxone did not modify, whereas sodium valproate significantly reduced the plasma GH and PRL rise during exercise. In the presence of sodium valproate, GH and PRL levels rose 3- and 1.5-fold, respectively, in response to exercise. When naloxone was given together with sodium valproate, both GH and PRL responses to exercise were abolished completely. These data suggest the involvement of a GABAergic mechanism in the regulation of GH and PRL responses to physical exercise in men. Furthermore, the data argue against a role of naloxone-sensitive endogenous opioids in the control of these hormonal responses to exercise, whereas they suggest a modulation by opioids of the GABAergic inhibitory action.

Vittorio Coiro, Istituto di Clinica Medica Generale e Terapia Medica, Università di Parma, via Gramsci 14, 43100 Parma, Italy

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V. Coiro, P. Chiodera, G. Rossi, R. Volpi, M. Salvi, L. Camellini and E. Roti

Abstract. iv administration of oxytocin decreases plasma ACTH-cortisol levels in normal men. In contrast, naloxone, a specific opioid antagonist, stimulates cortisol release, suggesting that opioid peptides exert an inhibitory control on ACTH-cortisol secretion.

The present study was carried out in an attempt to determine whether an opioid pathway mediates oxytocin action; therefore, we evaluated the effect of naloxone on the decrease of cortisol induced by oxytocin.

Six normal men were treated iv with oxytocin (2 IU as a bolus), naloxone (4 mg as a bolus plus 10 mg infused for 2 h) or a combination of the 2 drugs. Plasma cortisol levels were determined in samples taken before and 2 h after drug treatment. As expected, administration of oxytocin significantly decreased cortisol secretion, while naloxone had a stimulatory effect on plasma cortisol levels. When oxytocin injection was followed by administration of naloxone, cortisol levels remained unchanged; thus, naloxone abolished a cortisol decrement in response to oxytocin.

These findings show that in man oxytocin requires an active opioid system in order to produce its inhibitory action on ACTH-cortisol secretion, suggesting that this effect of oxytocin could be mediated by an opioid pathway.

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V Coiro, A Alboni, D Gramellini, C Cigarini, L Bianconi, D Pignatti, R Volpi and P Chiodera

The possible inhibition exerted by ethanol on the oxytocin response to breast stimulation was tested in normal women. The possible role of endogenous opioids in the control of the oxytocin response to breast stimulation and/or ethanol action was also examined. Sixteen normal women were tested four times on the 22nd day of four consecutive regular menstrual cycles. All women underwent mechanical breast stimulation (for 10 min) with the concomitant administration of normal saline, naloxone (2 or 4 mg in an iv bolus plus 5 or 10 mg over 16 min), ethanol (50 ml in 110ml of whisky po) or the combination of ethanol and naloxone. Plasma oxytocin levels rose about twofold after breast stimulation, with a mean peak response at 10 min. The oxytocin response to breast stimulation was not changed by the treatment with the lower (2 plus 5 mg) or the higher (4 plus 10 mg) dose of naloxone, whereas it was completely abolished by ethanol. However, when ethanol was given together with naloxone, the oxytocin rise induced by breast stimulation was only partially inhibited by ethanol (the mean oxytocin peak was 50% higher than baseline). At both doses naloxone produced similar effects. These data demonstrate that ethanol inhibits the oxytocin response to breast stimulation. Naloxone sensitive endogenous opioids do not appear to be involved in the control of the oxytocin rise induced by breast stimulation. In contrast, since naloxone partially reversed the inhibiting effects of ethanol, a partial involvement of opioid peptides in ethanol action is supposed.

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V. Coiro, M. Passeri, C. Davoli, A. Bacchi-Modena, L. Bianconi, R. Volpi and P. Chiodera

Abstract. The effect of oxytocin on the ACTH, cortisol, GH and PRL response to physical exercise was investigated in 6 normal men. In addition, the possible involvement of endogenous opioids in the mediation of oxytocin action was evaluated. After fasting overnight, each subject was tested on four mornings at least 1 week apart. Exercise was performed on a bicycle ergometer. The workload was gradually increased at 3-min intervals until exhaustion and lasted about 20 min in all subjects. Tests were carried out under administration of oxytocin (2000 mIU as an iv bolus injection plus 32 mIU/min per 30 min) or naloxone (10 mg as an iv bolus injection) alone; furthermore, the effect of oxytocin together with naloxone (10 mg as an iv bolus injection) was evaluated. In the remaining test, normal saline was given instead of drugs. Plasma ACTH, cortisol, PRL and GH concentrations were significantly increased by physical exercise. Administration of oxytocin, naloxone or their combination was without effect on the PRL and GH rise elicited by exercise. In contrast, the exercise-induced ACTH and cortisol response was significantly raised by naloxone and reduced by oxytocin. When oxytocin was preceded by administration of naloxone, the ACTH and cortisol response to exercise was not reduced by oxytocin. These data show that oxytocin is capable of inhibiting the rise in ACTH and cortisol, but not in GH and PRL induced by physical exercise. Since naloxone abolished the inhibitory effect of oxytocin, oxytocin action on ACTH and cortisol secretion might be supposed to be mediated by an opioid pathway. However, we cannot exclude that oxytocin and naloxone act at different sites in the hypothalamic-pituitary system.

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G Gerra, R Volpi, R Delsignore, L Maninetti, R Caccavari, S Vourna, D Maestri, P Chiodera, G Ugolotti and V Coiro

To establish a possible different reaction between the male and the female to short-term exposure to cold, thermal, cardiovascular and pituitary hormonal responses to cold stress were measured in eight normal men and eight women (ages 19–24). The women were eumenorrheic and were tested in the follicular phase. Each subject, lightly clad, was required to remain for 30 min in a room at an ambient temperature of 2 5°C followed by a 30 min period in a cold room at 4°C. A month later, control tests were carried out at a constant 25°C temperature for 1 h in the same subjects. Skin temperature, heart rate, blood pressure and plasma levels of beta-endorphin, ACTH, cortisol, GH and PRL were measured before and after cold exposure in the two groups. Before the test, all examined parameters were similar in the two groups. During cooling, blood pressure rose and pulse rate decreased significantly in the men, but not in the women, whereas skin temperature dropped in both groups. However, after cold exposure skin temperature was significantly lower in the women than in the men. A slight, but not significant increase in beta-endorphin, ACTH, cortisol and GH levels was observed after cooling in the men, whereas the women showed significant increments of these hormones, When values of skin temperature were combined with the differential (after minus before cold test) hormonal values, significant negative correlations were found for beta-endorphin, ACTH, cortisol and GH. As observed by other authors, a significant and peculiar cold-induced decline in plasma PRL levels was observed in the men; by contrast, a slight, but not significant decrement of PRL was found in the women. Control tests at a constant 25°C temperature did not show significant thermal, cardiovascular or hormonal changes in any subject. These data reflect stronger thermal, cardiovascular and PRL responses to cooling in men than in women. On the other hand, the women, but not the men, showed significant cold-stress-induced increments of beta-endorphin, ACTH and GH, suggesting that the more efficient adaptation to cold of the men might be what prevents the stress-induced hormonal changes observed in the women.

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V. Coiro, M. Passeri, G. Gelmini, C. Davoli, G. Bianconcini, R. Volpi, R. Minelli, P. Delia, F. Fagnoni and P. Chiodera

Abstract. The possible mediation of muscarinic and/or nicotinic-cholinergic receptors in the response of ACTH to insulin-induced hypoglycaemia was evaluated in 18 normal men. Subjects were tested with the insulin (0.15 U/kg) tolerance test (ITT) in basal conditions and in the presence of the M1- and M2-muscarinic antagonist atropine (600 μg iv just before insulin injection (time 0) plus 600 μg 20 min later in 6 subjects) or the M1-muscarinic receptor blocker pirenzepine (40 mg iv 10 min before ITT or 20 mg at time 0 plus 30 mg at time 20 in 6 subjects). The remaining 6 men were treated with the nicotinic receptor antagonist trimethaphan (0.3 mg/min × 30 min before ITT). ACTH rose 4.7 times in response to hypoglycaemia. The ACTH response to hypoglycaemia did not change after pirenzepine administration, whereas it was significantly increased by atropine and decreased by trimethaphan treatment. These data indicate that nicotinic and muscarinic (M2 but not M1) receptors participate in a different manner in the regulation of the hypoglycaemia-induced ACTH release.

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V. Coiro, R. Volpi, L. Capretti, G. Speroni, A. Castelli, A. Mosti, C. Marchesi, E. Gardini, G. Rossi and P. Chiodera

Abstract. The present study was undertaken in order to establish whether muscarinic cholinergic receptors are involved in the anomalous GH response to GnRH in men with insulin-dependent diabetes mellitus and in male patients with major depression. For this purpose, 16 male diabetics, 18 depressed men and 9 normal controls were tested with GnRH (25 μg iv) with and without previous treatment with the muscarinic cholinergic receptor blocker pirenzepine (40 mg iv 10 min before GnRH). Additional experiments with TRH (200 μg iv 10 min after pirenzepine) were performed in the same subjects and used for comparison between responders to TRH and GnRH. The administration of GnRH stimulated GH release in 12 out of the 16 diabetics and in 8 out of the 18 depressed patients, but not in the normal controls. Control and diabetic non-responders to GnRH did not respond to TRH. In contrast, all diabetic responders to GnRH, except 2, showed paradoxical GH responses to TRH. All depressed responders to GnRH and 3 of the non-responders, were responsive to TRH. The pattern and magnitude of the secretory responses to TRH and GnRH were similar in depressed and diabetic patients. When the effects of GnRH and TRH were restudied in the presence of pirenzepine, neither GnRH nor TRH enhanced the serum concentrations of GH in any patient. These data indicate that a muscarinic cholinergic mechanism is involved in the anomalous responses of GH to GnRH and TRH in diabetic men and in male patients affected by major depression.

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V. Coiro, R. Volpi, L. Capretti, A. Bacchi-Modena, C. Cigarini, L. Bianconi, G. Rossi, D. Gramellini and P. Chiodera


Arginine vasopressin responses to osmotic (0.1 ml · kg−1 · min−1 NaCl), orthostatic (standing upright and maintenance of orthostatic position for 20 min), and hypoglycemic (0.15 IU/kg insulin) stimuli were evaluated in women with polycystic ovaries and in normal subjects. Blood dehydroepiandrosterone, dehydroepiandrosterone sulphate, androstenedione, testosterone, cortisol, and endogenous insulin levels were significantly higher in women with polycystic ovaries than in controls, whereas estrone, estradiol-17β, progesterone and 17OH-progesterone concentrations were normal in all subjects. Arginine vasopressin basal levels (mean ± sem of 3 test days; women with polycystic ovaries: 2.8 ± 0.2 pmol/l; controls: 2.7 ± 0.2 pmol/l) and secretory responses to orthostatic (mean peaks 100% higher than baseline values) and to hypertonic (130% increments) stimuli were similar in the two groups. Arginine vasopressin responses to hypoglycemia were lower in women with polycystic ovaries (50% increment) than in controls (150% increment), although comparable blood glucose decrements and GH or cortisol increments were found in the two groups. Arginine vasopressin peak responses to hypoglycemia were negatively correlated to testosterone, androstenedione, and endogenous insulin levels, but did not correlate with basal and hypoglycemia-induced peak cortisol concentrations or with circulating levels of other steroids. These data indicate a hypothalamic posterior pituitary disorder affecting arginine vasopressin response to insulin-induced hypoglycemia in women with polycystic ovaries syndrome associated with elevated blood androgen and insulin concentrations.

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R. Volpi, P. Chiodera, L. Cerri, G. Roberti, G. Salati, P. Ferrari, R. Delsignore, G. Pedretti, L. d'Amato and V. Coiro

Abstract. In order to evaluate the possible involvement of muscarinic cholinergic receptors in the GH response to TRH in patients with liver cirrhosis, 8 males with post-hepatitic cirrhosis and 11 males with postalcoholic cirrhosis were primed with the anticholinergic agent pirenzepine and tested with TRH. In addition, 10 male patients affected by piecemeal necrosis were tested in a similar manner. High basal concentrations of GH were found in all groups. None of the patients with piecemeal necrosis responded to TRH, whereas in patients with post-hepatitic and in post-alcoholic cirrhosis, TRH induced a significant rise in GH levels. The priming with pirenzepine (40 mg given iv 10 min before TRH) completely blocked the TRH-induced GH increase, but did not affect the TRH-induced TSH release. These data suggest that a muscarinic cholinergic pathway is involved in the anomalous response of GH to TRH in patients with liver cirrhosis. The lack of effect of pirenzepine on the TRH-stimulated TSH release suggests that the muscarinic cholinergic mediation is peculiar for the effect of TRH on GH secretion.