7 results on '"Netti, C"'
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2. Influence of Brain Histaminergic System on Episodic Growth Hormone Secretion in the Rat.
- Author
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Netti, C., Guidobono, F., Olgiati, V.R., Sibilia, V., Pagani, F., and Pecile, A.
- Published
- 1982
- Full Text
- View/download PDF
3. Effects of amylin and salmon calcitonin on beta-endorphin-induced growth hormone and prolactin secretion in the rat.
- Author
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Pagani F, Netti C, Guidobono F, Lattuada N, Ticozzi C, and Sibilia V
- Subjects
- Amyloid antagonists & inhibitors, Amyloid metabolism, Animals, Binding Sites, Binding, Competitive, Calcitonin antagonists & inhibitors, Calcitonin metabolism, Cell Membrane metabolism, Growth Hormone blood, Hypothalamus metabolism, Injections, Intraventricular, Islet Amyloid Polypeptide, Male, Peptide Fragments pharmacology, Prolactin blood, Radioimmunoassay, Rats, Rats, Sprague-Dawley, Time Factors, Amyloid pharmacology, Calcitonin pharmacology, Growth Hormone metabolism, Prolactin metabolism, beta-Endorphin pharmacology
- Abstract
In this study we examined the possible interplay of amylin (AMY) and salmon calcitonin (sCT) in the central control of growth hormone (GH) and prolactin (PRL) secretion in male rats. For this purpose we first compared effects of central intracerebroventricular (i.c.v.) admininstration of various doses of AMY (2.5-2,500 ng/rat) and sCT (2.2-220 ng/rat) on beta-endorphin (beta-END, 0.5 microg/rat)-induced GH and PRL secretion. AMY and sCT dose-dependently inhibited beta-END-induced GH secretion, whereas only sCT was able to inhibit beta-END-induced PRL secretion. To examine whether the GH inhibitory effect of AMY was due to the possible cross-reactivity of AMY and sCT on the same receptors in the CNS, we pretreated some rats with the AMY antagonist (AMY8-37, 2. 5 microg/rat, i.c.v.). AMY8-37 significantly enhanced the GH-stimulatory action of beta-END. AMY8-37, administered prior to AMY and sCT, significantly removed the inhibitory effect of both AMY and sCT on beta-END-induced GH release, suggesting that both peptides mediate their response on GH through a common receptor. In vitro competition binding studies on rat hypothalamic membranes have shown that both AMY and sCT compete with [125I]rAMY binding with half inhibition (IC50) values of 3.6 x 10(-11) and 1.6 x 10(-10) M, respectively. Binding of [125I]sCT was inhibited by sCT with an IC50 of 1.09 x 10(-10) M and to a lesser extent by AMY with an IC50 of 1. 3 x 10(-6) M. Thus it is possible that the two peptides recognize a common hypothalamic receptor but with different affinities (sCT > AMY). Overall these data indicate that AMY behaves as a mimic of sCT in the central control of GH secretion. The failure of AMY, at variance with sCT, to modify the PRL-releasing activity of beta-END indicates that different receptor subtypes for sCT are involved in the endocrine effects of sCT and only those mediating the modulatory action of GH respond to AMY.
- Published
- 1998
- Full Text
- View/download PDF
4. Inhibitory effect of amylin on growth hormone responsiveness to growth-hormone-releasing hormone in the rat.
- Author
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Netti C, Sibilia V, Pagani F, Lattuada N, Coluzzi M, Pecile A, and Guidobono F
- Subjects
- Animals, Dose-Response Relationship, Drug, Injections, Spinal, Islet Amyloid Polypeptide, Male, Rats, Rats, Sprague-Dawley, Time Factors, Amyloid pharmacology, Brain drug effects, Growth Hormone metabolism, Growth Hormone-Releasing Hormone pharmacology
- Abstract
The effects of intracerebroventricular (i.c.v.) or intracarotid (i.a.) administration of amylin (AMY) on growth hormone (GH) release induced by GH-releasing hormone (GHRH) were examined in conscious male rats. Amylin (25 ng-5 micrograms/rat, i.c.v. or 10 micrograms/rat, i.a.) was administered 10 min before GHRH (2 micrograms/kg, i.a.). I.c.v. administration of AMY dose-dependently inhibited GH secretion induced by GHRH but when given peripherally, AMY did not modify the GH response to GHRH. Amylin (10(-8)-10(-6) M) had no direct effect on the rat anterior pituitary in vitro either alone or when incubated with GHRH. To characterize the mechanism(s) involved in vivo in the inhibition of GH by AMY, we examined, at first, the effects of AMY on GHRH-induced GH release in rats depleted of somatostatin by pretreatment (4 h before) with cysteamine (300 mg/kg s.c.). The inhibitory activity of AMY on GH secretion elicited by GHRH seems to be independent of hypothalamic somatostatin; in fact, AMY was still active in rats treated with cysteamine. In addition, we examined the effects of i.c.v. AMY administration on clonidine (CLO)-induced GH secretion and on dopamine and noradrenaline content in the brain, since it is known that GHRH is a stimulus sensitive to changes in central catecholaminergic activity. The failure of AMY to affect GH secretion induced by activation of postsynaptic alpha 2-receptors by CLO and the finding that the peptide decreased noradrenaline content in the hypothalamus and striatum, indicates that AMY may inhibit GH release by interfering with the facilitatory influence of the catecholaminergic system on GH secretion.
- Published
- 1995
- Full Text
- View/download PDF
5. Influence of brain histamine on growth hormone secretion induced by alpha-2-receptor activation.
- Author
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Netti C, Sibilia V, Guidobono F, and Pecile A
- Subjects
- Animals, Clonidine pharmacology, Cysteamine pharmacology, Injections, Intraventricular, Male, Radioimmunoassay, Rats, Rats, Sprague-Dawley, Receptors, Adrenergic, alpha-2 drug effects, Receptors, Presynaptic drug effects, Somatostatin antagonists & inhibitors, Brain Chemistry physiology, Growth Hormone metabolism, Histamine physiology, Receptors, Adrenergic, alpha-2 physiology
- Abstract
The effects of histamine (HA) and of (R) alpha-methyl-histamine (alpha-MeHA; a drug that decreases histaminergic tone through activation of presynaptic H3 receptors) on growth hormone (GH) secretion induced by clonidine (CLO), an alpha 2-adrenergic agonist, were examined in rats. HA (0.1 mumol/rat intracerebroventricularly) and alpha-MeHA (10 mg/kg i.a.) were administered 5 min and 3 h, respectively, before CLO (0.25 mg/kg i.a.). Blood samples for hormone determination were drawn from freely moving rats at various times before and after drug treatment. To characterize the mechanisms underlying the inhibition of GH secretion by HA, the effect of HA on GH induced by CLO was examined in rats depleted of catecholamine by pretreatment (2 h before) with alpha-methyl-p-tyrosine (alpha-MpT, 200 mg/kg s.c.) and in rats depleted of somatostatin by pretreatment (4 h before) with cysteamine (300 mg/kg s.c.). HA completely suppressed the GH-releasing effect of CLO whereas alpha-MeHA significantly enhanced the GH response to CLO. Neither alpha-MpT nor cysteamine pretreatment modified the inhibitory activity of HA on GH secretion elicited by CLO. The present results indicate that the inhibitory activity of brain HA on GH release consequent to activation of central alpha 2-receptors does not involve a modulatory action on catecholaminergic or somatostatinergic neurons but probably other mechanisms like the modulation of neurons synthetizing GH-releasing hormone.
- Published
- 1993
- Full Text
- View/download PDF
6. Cimetidine-induced prolactin release: possible involvement of the GABA-ergic system.
- Author
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Sibilia V, Netti C, Guidobono F, Pagani F, and Pecile A
- Subjects
- Animals, Diazepam pharmacology, Imidazoles pharmacology, Impromidine, Male, Pituitary Gland, Anterior metabolism, Rats, Rats, Inbred Strains, Receptors, Histamine H1 drug effects, Synaptic Transmission drug effects, gamma-Aminobutyric Acid pharmacology, Cimetidine pharmacology, Pituitary Gland, Anterior drug effects, Prolactin metabolism, gamma-Aminobutyric Acid physiology
- Abstract
The mechanism of cimetidine-induced prolactin (PRL) release was studied. Intracarotid (i.a.) administration of 1 mg/kg of impromidine, the most specific H2 histamine agonist known, did not counteract the cimetidine-induced hypersecretion of PRL. Pre-treatment with benzodiazepines (diazepam or lorazepam, 3 mg/kg/i.a.) completely suppressed it. Administration of gamma-aminobutyric acid (GABA 5 mg/kg/i.a.) was also able to prevent it, but to a lesser extent than benzodiazepines. Simultaneous administration of doses of diazepam (1.5 mg/kg/i.a.) and GABA (3 mg/kg/i.a.) ineffective per se markedly blunted the increase of PRL by cimetidine. We conclude that cimetidine does not induce hypersecretion of PRL by its action on histamine H2 receptors, but through other pharmacological activities of the drug, such as perhaps interaction with the GABA-ergic system in the pituitary.
- Published
- 1985
- Full Text
- View/download PDF
7. Evidence of a central inhibition of growth hormone secretion by calcitonin gene-related peptide.
- Author
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Netti C, Guidobono F, Sibilia V, Pagani F, Braga PC, and Pecile A
- Subjects
- Animals, Calcitonin Gene-Related Peptide, Growth Hormone antagonists & inhibitors, Injections, Intra-Arterial, Injections, Intraventricular, Male, Neuropeptides administration & dosage, Rats, Rats, Inbred Strains, Calcitonin pharmacology, Growth Hormone metabolism, Neuropeptides pharmacology
- Abstract
The effects of intracerebroventricular or intracarotid injection of synthetic rat calcitonin gene-related peptide (CGRP) on growth hormone (GH) secretion induced by various stimuli in male rats were examined. CGRP (2.5 or 5 micrograms/rat intracerebroventricularly, i.c.v.) was administered 10 min before beta-endorphin (0.5 microgram/rat i.c.v.) or morphine (1 mg/kg intracarotidly, i.a.) or clonidine (0.25 mg/kg i.a.) or GH-releasing hormone (GHRH1-40; 2 micrograms/kg i.a.). When injected peripherally, CGRP (10 micrograms/rat, i.a.) was administered 5 min before morphine or GHRH. To investigate the possible involvement of somatostatin (SRIF) in the inhibition of GH secretion by CGRP, the effect of the peptide on GHRH-induced GH release was also examined in rats with hypothalamic SRIF depletion obtained by pretreatment (4 h before) with cysteamine (300 mg/kg subcutaneously). Blood samples for hormone determination were drawn from freely moving rats at various times before and after drug treatment. The intracerebroventricular administration of CGRP (5 micrograms/rat) significantly inhibited GH secretion induced by all the stimuli used. In rats with SRIF depletion CGRP did not modify the stimulation of GH by GHRH. When CGRP was administered intracarotidly, even the dose of 10 micrograms/rat did not reduce the GH release induced by GHRH or morphine. The effects of intracerebroventricular CGRP on basal or beta-endorphin-induced prolactin release were also examined. When given intracerebroventricularly, the peptide did not modify prolactin secretion. The present results indicate that CGRP has a central inhibitory role in the control of GH secretion, probably through a stimulation of SRIF release.
- Published
- 1989
- Full Text
- View/download PDF
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