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Biomedical subjects

V Coiro

Publications and source records attributed to V Coiro.

At least 181 records · Page 10Linked to original sources
PubMed1985

Effect of naloxone on oxytocin-induced cortisol decrease in normal men.

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.

Adrenocorticotropic Hormone↗
PubMed1985

Inhibition by somatostatin of the release of growth hormone induced by lysine-vasopressin in normal subjects.

The effect of somatostatin (SRIH) on the release of growth hormone (GH) induced by lysine-vasopressin (LVP) was studied in six normal subjects. They were injected intravenously with 0.06 I. U./kg of LVP alone or in combination with SRIH (an intravenous bolus of 100 micrograms 10 minutes before LVP injection, followed by the constant infusion of 500 micrograms over 90 minutes). LVP strikingly increased serum concentrations of GH; this response was significantly reduced by the treatment with SRIH. This finding provides evidence that the effect of LVP on serum GH levels is sensitive to the inhibition by SRIH; it is proposed that the stimulating action of LVP on GH secretion might be mediated by the inhibition of endogenous SRIH.

Adult↗
PubMed1984

Plasma levels and renal removal of gastrin after acute hepatic ischemia in dogs.

Plasma levels and renal uptake of gastrin were determined in ten dogs submitted to complete liver devascularization in order to induce an acute liver failure. Renal function was evaluated by renal plasma flow (RPF) and glomerular filtration rate (GFR) determinations. Liver devascularization was obtained by end-to-side porto-caval shunt (PCS) followed by temporary clamping of the hepatic artery. PCS alone did not affect renal function and renal ability to remove gastrin; after hepatic ischemia, both RPF, GFR and renal extraction of gastrin showed an abrupt decrease. At the end of the period of hepatic ischemia 5 dogs were submitted to glucose infusion, in consideration that: i) glucagon is able both to affect gastrin release and renal hemodynamics, and ii) hypoglycemia that develops after liver failure releases elevated amounts of glucagon. The renal handling of gastrin was not related to glucagon plasma levels, though the higher gastrin levels occurred at the lower glucagon concentrations. These data suggest that in acute liver failure there is a striking decrease of the renal clearance of gastrin associated with the impairment of kidney function. Furthermore, in this pathological condition plasma gastrin levels are affected by blood glucose concentrations through its effect on plasma glucagon levels.

Acid-Base Equilibrium↗
PubMed1984

Evaluation of oxytocin administration on luteinizing hormone and follicle-stimulating hormone response to luteinizing hormone-releasing hormone during the menstrual cycle of normal women.

In order to determine whether oxytocin modifies luteinizing hormone (LH) and follicle-stimulating hormone (FSH) secretion in response to LH-releasing hormone (LH-RH), a group of normal women, 23 to 30 years of age, was studied in the follicular, periovulatory, and luteal phases. LH and FSH response to LH-RH was evaluated in the serum under control conditions and after oxytocin infusion. Oxytocin administration failed to modify LH and FSH release induced by LH-RH. These results suggest that this neuropeptide is not involved in the control of LH and FSH at the level of the anterior pituitary.

Adult↗
PubMed1984

Different effects of metoclopramide and domperidone on GH release in type I male diabetics.

Dopamine (DA) has a physiological role in the control of GH release from the pituitary. Studies have been carried out using DA agonist or antagonist, since in normal subjects DA does not cross the blood-brain-barrier (BBB). In contrast, the BBB is altered in type I diabetics, who respond to DA with a significant increase of GH release. In these patients Metoclopramide (MCP), an antidopaminergic drug, is also capable of stimulating GH release. In a previous paper, we suggested that this effect could be related to enhanced blood concentrations of DA, due to a reduced peripheral DA catabolism determined by MCP. However, since MCP crosses the BBB, an effect of this drug on other hypothalamic neurotransmitters could not be excluded. The purpose of the present study was to determine whether Domperidone (DOM) a drug which does not cross the BBB, but as well as MCP is thought to increase blood levels of DA, is also capable of inducing GH release in diabetics. Sixteen type I male diabetics were injected intravenously with MCP (6) or DOM (10) and a week later with normal saline. Ten normal subjects participated as controls to all three tests. MCP and DOM did not produce any effects in the normal controls; as expected, MCP induced a marked increase in serum levels of GH in the diabetics, while in contrast DOM did not stimulate GH secretion in diabetics. These data suggest that the effect of MCP is not due to the dopaminergic pathway previously described, but rather to a modulation of some other neurotransmitter at hypothalamic level, or to a direct effect on the pituitary in diabetics.

Adult↗
PubMed1984

Nicotine from cigarette smoking enhances clonidine-induced increase of serum growth hormone concentrations in men.

In order to determine whether nicotine exerts its stimulant effect on serum concentrations of growth hormone (GH) by interacting with an adrenergic pathway, we evaluated the effect of cigarette smoking on the response of GH to the administration of clonidine, a specific alpha-adrenoceptor agonist. In six normal volunteers, clonidine significantly increased serum levels of GH. When subjects smoked two non-filter cigarettes, GH response to the alpha-adrenoceptor agonist was greatly enhanced. These findings suggest that in man nicotinic cholinergic and adrenergic mechanisms might interact in the stimulation of GH secretion.

Adult↗
PubMed1984

Effect of pharmacological doses of oxytocin on insulin response to glucose in normal man.

In this study we have examined the effect of the administration of oxytocin on basal blood concentrations of insulin, glucagon, cortisol, growth hormone, and on the dynamic secretory response of these hormones to intravenous glucose administration (0.33 g/kg) in basal condition and after the injection of 3 IU (1 plus 2 IU/1 h) or 6 IU (2 plus 4 IU/1 h) of oxytocin (6 subjects for each group). The highest dose of oxytocin (6 IU) used significantly increased insulin secretion in response to intravenously administered glucose. No significant change of insulin secretion was observed with 3 IU of oxytocin. Glucagon, cortisol, and growth hormone response to intravenous injection of glucose was not affected by oxytocin (3 or 6 IU) administration. These results suggest that high doses of oxytocin affect beta-cell function in normal man.

Adult↗
PubMed1984

The growth hormone response to thyrotropin-releasing hormone in insulin-dependent diabetics involves a cholinergic mechanism.

In order to establish whether cholinergic receptors mediate GH secretion induced by TRH in insulin-dependent diabetes, 10 patients were treated with pirenzepine, an anticholinergic agent, and tested with TRH. Basal concentrations of GH were elevated in these patients and 8 of 10 patients responded to TRH with a significant rise in GH levels. Pretreatment with pirenzepine (40 mg given iv 10 min before TRH) suppressed the TRH-induced GH rise. Pirenzepine had no effect on TRH-induced TSH release. This finding suggests that a cholinergic mechanism is involved in the paradoxical response of GH to TRH in diabetic patients.

Adult↗
PubMed1984

Histaminergic H1 and H2 receptors do not mediate cortisol release in response to naloxone in normal men.

In order to evaluate the role of histamine as a possible mediator of the ACTH-cortisol response to naloxone, a specific opioid receptor antagonist, 12 normal men were treated with naloxone before and after the administration of dexchlorpheniramine and cimetidine, respectively H1 and H2 histamine receptor antagonists. Cortisol levels in the plasma were measured before and after drug injections. Naloxone significantly stimulated the secretion of cortisol in all subjects; the administration of dexclorpheniramine or cimetidine failed to modify this response. These data confirm the stimulatory effect of naloxone on cortisol secretion, but do not support the hypothesis that a histaminergic pathway mediates this response.

Adrenocorticotropic Hormone↗
PubMed1983

Naloxone does not alter the effect of gamma aminobutyric acid derivative, baclofen, on GH release in man.

To evaluate the interaction between opioid peptides and GABAergic system in regulating GH secretion we administered 5 mg of baclofen, a GABA derivative, to eight normal male subjects. The results were compared to those obtained in the same subjects treated with naloxone (10 mg/2 h) plus baclofen. GH levels increased significantly above basal value either after baclofen and naloxone plus baclofen without any significant difference between GH responses during the two tests. It is suggested that the two substances do not act at the level of the same receptor site. The evaluation of a possible interaction between opioid peptides and GABAergic system on GH release requires further investigation.

Adult↗
PubMed1983

Effect of metoclopramide on serum growth hormone levels in cirrhotic men.

Growth hormone (GH) secretory response to metoclopramide (MCP) administration was evaluated in 9 male patients with liver cirrhosis and in 6 normal controls. As expected, MCP did not modify serum GH concentrations in normal subjects. In contrast, a striking GH secretory response to MCP was observed in 5 out of 9 cirrhotics. In the other four patients serum GH levels did not show any variation after MCP. The different behavior between cirrhotic "responders" and "non responders" can not be interpreted on the basis of the medical history or the clinical and laboratory data. Three hypothesis are proposed: i) The effect of MCP could be promoted by estrogens and inhibited by androgens. ii) False neurochemical transmitters could affect dopaminergic system of some cirrhotics, allowing or inhibiting the GH response to MCP. iii) MCP could stimulate GH secretion by a serotonergic mechanism. These findings provide further evidence of a modification of the GH secretory pattern in patients with cirrhosis of the liver.

Adult↗