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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
PubMed1987

Cholinergic mediation of growth hormone secretion induced by thyrotropin-releasing hormone in cirrhotic patients.

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 post-alcoholic 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.

Adult↗
PubMed1987

Nicotinic and M1-, M2-muscarinic cholinergic control of ACTH response to insulin-induced hypoglycaemia in man.

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 micrograms iv just before insulin injection (time 0) plus 600 micrograms 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 x 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.

Adrenocorticotropic Hormone↗
PubMed1987

Oxytocin enhances thyrotropin-releasing hormone-induced prolactin release in normal menstruating women.

The effects of oxytocin (OT) on basal thyrotropin-releasing hormone (TRH)-stimulated thyrotropin (TSH) and prolactin (PRL) secretion were evaluated in normal menstruating women during follicular, periovulatory, and luteal phases. Two different studies were performed. In one study, 15 subjects were treated with OT or saline; in the other study, 20 women were tested with TRH alone or in combination with OT. Results during follicular, periovulatory, and luteal phases were similar. OT did not produce any effect on basal serum TSH and PRL levels and on the TRH-stimulated TSH secretion, whereas it significantly enhanced the PRL response to TRH. At all examined phases during the menstrual cycle, the mean peak PRL response was reached within 20 minutes after TRH injection, and the peak was about three times higher than basal value when TRH was given alone and about four times when OT was present. These data suggest that in normal women OT is not involved in the control of basal and TRH-stimulated TSH secretion and of basal PRL release. In contrast, the enhancement of the TRH-induced PRL release suggests that OT plays a role in the control of the acutely stimulated PRL secretion. Because results were similar regardless of the phase of the menstrual cycle, estrogen and/or progesterone do not appear to be involved in the effect of OT on the TRH-induced PRL release.

Adult↗
PubMed1986

Muscarinic cholinergic modulation of insulin response to an intravenous glucose tolerance test in normal man.

The effect of pirenzepine, a specific muscarinic cholinergic receptor antagonist, on insulin and glucagon responses to an intravenous injection of glucose was investigated in eight normal adult subjects. These volunteers received two iv glucose tolerance tests (0.33 g/kg) before and after the oral administration of 125 mg of pirenzepine (three doses of 25 mg during the day before the experiment and a fourth dose of 50 mg 2 h before glucose injection). Treatment with pirenzepine neither altered basal blood glucose levels nor affected glucose tolerance after the injection of the glucose load. In addition, it did not modify basal plasma insulin and glucagon levels and the decrement of glucagon in response to glucose injection. In contrast, pirenzepine significantly decreased insulin release induced by glucose administration. In man, during the present experimental conditions, the muscarinic cholinergic system modulates insulin, but not glucagon response to an iv glucose injection.

Adult↗
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↗