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Biomedical subjects

R Volpi

Publications and source records attributed to R Volpi.

At least 145 records · Page 8Linked to original sources
PubMed1986

Nicotinic-cholinergic involvement in arginine-vasopressin response to insulin-induced hypoglycemia in normal men.

In order to establish whether arginine-vasopressin (AVP) release in response to insulin-induced hypoglycemia is mediated by a muscarinic and/or nicotinic cholinergic pathway, 12 normal men had an insulin tolerance test (ITT) in basal conditions and after treatment with the muscarinic receptor blocker pirenzepine (40 mg IV (intravenously) ten minutes before ITT in six subjects) or the nicotinic receptor antagonist trimethaphan (0.3 mg/min X 30 min IV before ITT in six subjects). The drugs did not modify arterial blood pressure nor produce side effects capable of altering AVP secretion. Pirenzepine administration did not change AVP response to hypoglycemia, whereas trimethaphan significantly reduced AVP increase by about 50% during the ITT. These data suggest the involvement of a cholinergic-nicotinic mechanism in regulation of AVP response to hypoglycemia.

Adult↗
PubMed1986

Different effects of metoclopramide and domperidone on arginine-vasopressin secretion in man.

This study was performed in order to investigate the dopaminergic mechanism involved in the control of arginine-vasopressin (AVP) secretion in normal men. Plasma AVP concentrations were measured before and after the administration of an i.v. bolus of 10 mg metoclopramide or domperidone to twelve healthy males. Metoclopramide, a cerebral and peripheral antagonist of dopaminergic receptors, significantly stimulated AVP secretion, whereas domperidone, a dopamine antagonist which does not cross the blood-brain barrier, was without effect. These data suggest that metoclopramide stimulates the release of AVP by blocking dopaminergic receptors in structures located inside the blood-brain barrier. Alternatively, it is possible that the stimulation of AVP release induced by metoclopramide does not occur through inhibition of dopamine receptors but rather through interaction with other neuroendocrine pathways.

Adult↗
PubMed1986

Inhibition by somatostatin of LH-RH-induced LH release in normal menstruating women.

The present study was carried out in order to establish whether the concomitant treatment with somatostatin (SRIH) is capable of modifying gonadotrophin release in response to LH-RH administration in normal women during follicular, periovulatory, and luteal phases. SRIH was administered in a dose of 5.55 micrograms/min over 180 min and LH-RH (100 micrograms) was injected as a bolus at 90 min after the beginning of SRIH infusion. Within the dose used, SRIH significantly reduced LH response to LH-RH, whereas it did not alter FSH response to LH-RH. These results suggest that SRIH may play a part in the regulation of LH secretion in normal women.

Adult↗
PubMed1985

Thyrotropin-releasing hormone does not inhibit lysine vasopressin-induced growth hormone secretion in normal men.

In order to establish whether thyrotropin-releasing hormone (TRH) inhibits lysine-vasopressin (LVP)-induced growth hormone (GH) release, six normal men were tested with LVP alone or in combination with TRH. LVP strikingly increased serum GH levels; this response was not altered by TRH. These results indicate that in man TRH is not involved in the control of GH secretion in response to LVP.

Adult↗
PubMed1985

Muscarinic cholinergic mediation of LHRH-induced LH and FSH secretion in normal men.

LHRH (100 micrograms i.v. bolus) was given to six young healthy men under basal conditions and after the administration of pirenzepine (10, 20, 30 or 40 mg i.v. 10 min before LHRH), which is a selective blocker of muscarinic cholinergic receptors. Pretreatment with 10 mg of pirenzepine did not modify LH and FSH responses to LHRH, whereas larger amounts of the drug significantly reduced gonadotrophin responses to LHRH. A dose-related effect of the drug was not observed, since a maximal reduction of LHRH-induced gonadotrophin secretion was already present when 20 mg of pirenzepine were used. When the effect of pirenzepine (20 mg) on the basal concentrations of FSH and LH was studied in four additional sex and age matched subjects, no significant changes were observed for at least 120 min after the injection. These results demonstrate that LHRH-induced LH and FSH secretion involves a muscarinic cholinergic mechanism.

Adult↗
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↗
PubMed1984

Lung function among asbestos cement factory workers: cross-sectional and longitudinal study.

Ventilatory capacity tests and standardized respiratory questionnaires were used in 1973 and in 1980 to measure the effect of mixed dust exposure in the asbestos cement industry on respiratory symptoms and lung function in 65 exposed workers and 30 controls (exposed to polyvinyl chloride but not to asbestos). Workers exposed to asbestos had 1) a higher prevalence of breathlessness and chest pain, and a higher incidence of breathlessness; 2) lower 1980 values of forced vital capacity (FVC) (0.27-0.83 liters) and forced expiratory volume in 1 sec (FEV1) (0.23-0.62 liters); and 3) a faster decline (nearly 40 ml/year) in FVC and FEV1 between 1973 and 1980. The FVC annual decrease was 52.5 ml in the subjects with more than 15 years since first asbestos exposure, whereas it was 24.3 ml in those with less than 15 years, suggesting a faster decline after 15 years of exposure. The effect of asbestos exposure and smoking habits was less than additive as regards pulmonary function.

Adult↗
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

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↗