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Biomedical subjects

P Chiodera

Publications and source records attributed to P Chiodera.

At least 145 records · Page 8Linked to original sources
PubMed1988

Dopaminergic control of TSH secretion in endogenous depression.

To evaluate whether the inhibitory control exerted by endogenous dopamine on thyroid-stimulating hormone (TSH) secretion is altered in patients with major depressive disorder, 11 depressed patients and 9 normal controls were tested with the dopaminergic receptor antagonist domperidone (10 or 20 mg i.v.). The administration of domperidone induced a significant increase in circulating TSH levels in the normal controls, but not in the depressed patients. These data excluded the possibility that the dopaminergic inhibition of TSH secretion is enhanced in depression. To establish whether domperidone failure was due to a reduced dopaminergic tone, domperidone was administered before stimulation of TSH secretion with thyrotropin-releasing hormone (TRH) (200 micrograms i.v.). The TSH response to TRH was significantly lower in the depressed than in the control subjects, regardless of domperidone priming. However, in both groups domperidone enhanced the TRH-induced TSH release by 50%. These data suggest that the dopaminergic control of TSH secretion is not altered in patients with endogenous depression and that a reduced capacity of the pituitary to secrete TSH might be responsible for the reduced TSH responsiveness to TRH and domperidone.

Adult↗
PubMed1988

Inhibitory action of exogenous oxytocin on plasma cortisol in normal human subjects: evidence of action at the adrenal level.

In previous studies we demonstrated that exogenous oxytocin induces a decrease of basal and stimulated cortisol and ACTH plasma levels in the normal male. To rule out the possibility that oxytocin could also act at the adrenal level, we tested, in the present work, the influence of exogenous oxytocin on the cortisol increase secondary to the intravenous injection of a supraphysiological dose (0.25 mg) of synthetic ACTH1-24 (Synachten) in 9 normal male volunteers. We demonstrate that oxytocin infusion does not modify the ACTH plasma levels but, however, induces a decreased cortisol response to ACTH1-24. These results support the hypothesis that, beside its hypophysial inhibitory action on ACTH release, oxytocin acts also at the adrenal gland level to decrease cortisol release and/or synthesis in normal human subjects.

Adrenal Glands↗
PubMed1988

Oxytocin reduces exercise-induced ACTH and cortisol rise in man.

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.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenocorticotropic Hormone↗
PubMed1987

Oxytocin reduces metyrapone-induced ACTH secretion in human subjects.

The inhibitory action of oxytocin (OT) on adrenocorticotropin (ACTH) secretion has been disputed. Thus we evaluated the effect of exogenous OT on the elevated blood ACTH levels in normal human subjects. Metyrapone, a blocker of cortisol secretion, was given to enhance ACTH release. This experimental model was chosen because metyrapone-induced ACTH activation depends on diminution of the negative feed-back of cortisol, which is an important physiological mechanism in the control of ACTH secretion. A striking decline in plasma cortisol levels and a 10-fold rise in the mean plasma ACTH concentration was observed within 20 h after the beginning of metyrapone treatment (750 mg orally every 4 h). The administration of OT (2 IU as a i.v. bolus plus 4 IU infused in 2 h) significantly reduced the metyrapone-induced plasma ACTH rise. Since the effect of OT was evident when ACTH secretion was enhanced by a reduced cortisol-dependent negative feed-back, confirmation of the inhibitory action of OT on the ACTH secretory system in man is provided.

Adrenocorticotropic Hormone↗
PubMed1987

Naloxone decreases the inhibiting effect of ethanol on the release of arginine-vasopressin induced by cigarette smoking in man.

In order to establish whether ethanol exerts its inhibiting effect on the nicotine-induced release of arginine-vasopressin (AVP) by interacting with an opioid pathway, six normal volunteers were treated with naloxone (2 or 4 mg as IV bolus, plus 5 or 10 mg infused over 105 minutes) during (2 nonfilter) cigarette smoking and ethanol (50 mL to 110 mL of whiskey) drinking. In addition, control experiments with naloxone, ethanol, or cigarette smoking alone were performed. When given alone, naloxone and ethanol did not modify AVP secretion, whereas nicotine increased plasma AVP levels by about 2.5-fold. This effect was completely blocked by ethanol. In the presence of naloxone, AVP rose only by about 1.7-fold in response to nicotine. Since naloxone only partially reversed the inhibiting effects of ethanol, only a partial involvement of opioid peptides in ethanol action might be supposed. Alternatively, ethanol and naloxone-sensitive opioids might produce their inhibiting effects on AVP rise in response to nicotine through independent pathways.

Adult↗
PubMed1987

Lack of effect of bromocriptine and domperidone on arginine-vasopressin response to insulin-induced hypoglycemia in normal men.

In order to establish whether the arginine-vasopressin (AVP) increase evoked by insulin-induced hypoglycemia is mediated by a dopaminergic pathway, 16 normal men were given an insulin tolerance test (ITT) under basal conditions and after treatment with the dopamine agonist bromocriptine (2.5 mg by mouth) (eight subjects) or the dopamine antagonist domperidone (10 mg i.v.) (eight subjects). In addition, five out of eight subjects in each group were treated with higher doses of bromocriptine (5 mg by mouth) or domperidone (20 mg i.v.). Basal and ITT-stimulated AVP secretion was not modified by the drug treatments, suggesting that dopamine is not involved in the regulation of AVP secretion in response to insulin-induced hypoglycemia.

Adult↗
PubMed1987

Pirenzepine inhibits growth hormone, but not thyrotropin response to thyrotropin-releasing hormone in patients with endogenous depression.

In order to evaluate whether in endogenous depression the anomalous growth hormone (GH) response to thyrotropin-releasing hormone (TRH) is mediated by muscarinic cholinergic receptors, 12 patients were tested with TRH (200 micrograms iv) with and without previous treatment with the muscarinic cholinergic receptor blocker pirenzepine (40 mg iv 10 min before TRH). Control tests with normal saline also were performed. Administration of normal saline did not alter serum GH levels. In contrast, TRH injections significantly increased serum GH concentrations by about three-fold. This response was inhibited by pretreatment with pirenzepine. Another neuroendocrine marker of endogenous depression, the low TSH increase in response to TRH (delta less than or equal to 7 microU/ml), was observed in our patients. Pretreatment with pirenzepine did not modify this response. These data indicate that in patients with endogenous depression a muscarinic cholinergic mechanism is involved in the GH response but not in the TSH response to TRH.

Adult↗
PubMed1987

Involvement of a dopaminergic mechanism in the response of growth hormone to thyrotropin releasing hormone in patients with major depression.

In an attempt to establish whether, in patients with major depression, dopaminergic receptors are involved in the release of growth hormone (GH) induced by thyrotropin releasing hormone (TRH), eleven subjects were tested with TRH (200 micrograms in an i.v. bolus) with or without concomitant treatment with domperidone (10 mg in an i.v. bolus 10 min before TRH), an antidopaminergic agent which does not readily cross the blood-brain barrier. In 7 out of the 11 patients, TRH strikingly increased GH levels (responders) (the mean peak level was 9 times higher than basal value), whereas it was without effect in the remaining 4 patients (non-responders). When the responders were treated with domperidone before TRH injection, TRH-induced GH increase was still present, but it was significantly lower (the mean peak level was 5.3 times higher than basal value) than in the TRH test (p less than 0.02). These data suggest that the paradoxical response of GH or TRH in patients with major depression involves a dopaminergic mechanism active at sites situated outside the blood-brain barrier.

Adult↗
PubMed1987

Effect of obesity and weight loss on the arginine vasopressin response to insulin-induced hypoglycaemia.

Arginine vasopressin (AVP) response to insulin-induced hypoglycaemia was evaluated in 16 men with normal weight and in 9 obese men. Obese subjects were restudied following substantial weight loss. The decrease in blood glucose concentrations after insulin injection (0.15 U/kg i.v. bolus) had a similar pattern and magnitude in the normal controls and in the obese subjects both before and after weight loss. Basal plasma insulin concentrations in the obese patients were significantly higher than in the normal weight subjects, but were back to normal after weight reduction. During all tests, blood osmolality, haematocrit and blood pressure remained constant. The AVP rise during the insulin tolerance test (ITT) was significantly lower in the obese patients than in the normal controls. The mean peak plasma AVP level was 2.3 times higher than the basal value in the normal controls, but only 1.6 times in the obese patients. After weight loss, the obese men regained normal AVP responses during the ITT. These data indicate that a hypothalamic pituitary disorder affects the AVP response to insulin-induced hypoglycaemia in obese men.

Adult↗
PubMed1987

Muscarinic cholinergic and histaminergic H1 and H2 receptors are not involved in the LH response to naloxone in man.

The role of muscarinic-cholinergic and H1-, H2-histaminergic receptors as possible mediators of the LH response to the opioid antagonist naloxone was evaluated in 18 normal men. Subjects were divided in 3 groups of 6 men; the increment of LH in the plasma elicited by naloxone was evaluated after giving naloxone alone or together with dexchlorpheniramine, cimetidine or pirenzepine (respectively H1-, H2-histaminergic and muscarinic-cholinergic receptor antagonists). LH release was significantly stimulated by naloxone in all subjects; this response was not altered by histaminergic or cholinergic blockade. These results confirm the stimulatory effect of naloxone on LH release in man, without evidence of the involvement of H1-, H2-histaminergic or muscarinic-cholinergic pathways.

Adult↗
PubMed1987

TSH and PRL responses to domperidone and TRH in men with insulin-dependent diabetes mellitus of different duration.

The effect of domperidone, a specific blocker of dopamine receptors, on serum TSH and PRL levels was evaluated in 16 euthyroid men affected by insulin-dependent diabetes mellitus (IDDM) of different duration and in 7 age-matched normal controls. Diabetics were divided into 2 groups of 8 men according to the duration of their disease (group I: 1-9 years; group II: 11-18 years). Both groups had normal basal levels of TSH and PRL. Responses of these hormones to domperidone were similar in normal controls and in group I diabetics, whereas they were significantly reduced in patients of group II. When all 16 diabetics were studied together, a significant negative correlation was found between mean maximal peaks of TSH and PRL responses to domperidone and duration of diabetes. In order to evaluate whether the reduced effect of domperidone in diabetics was due to alterations of the dopaminergic control of TSH and PRL secretion, the domperidone test was repeated in 6 normal controls and in 6 diabetics of group II after infusion of dopamine (4 micrograms/kg/min for 2 h). Dopamine infusion induced parallel decreases in TSH and PRL concentrations, without modifying hormonal secretory patterns in response to domperidone. These data suggested that the reduced TSH and PRL responses to domperidone in diabetics were not due to alterations of the dopaminergic control of pituitary function but to a defect at the pituitary level. To test this hypothesis, TSH and PRL responses to TRH were evaluated in group I and group II diabetics and in normal controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Lysine-vasopressin does not affect basal and LH-RH-stimulated LH and FSH release during the menstrual cycle of normal women.

In order to test possible effects of lysine-vasopressin (LVP) on basal and LH-RH-stimulated LH and FSH release, an intravenous bolus of LVP (0.06 IU/kg body weight) was injected alone or 10 min before LH-RH (100 micrograms i.v.) in 33 normal women in the follicular, periovulatory and luteal phase of their menstrual cycle. The administration of LVP modified neither the basal secretion of the gonadotropins nor the LH-RH-induced LH and FSH release. These data suggest that in humans, vasopressin is not involved in the control of gonadotropin release at the level of the anterior pituitary.

Adult↗
PubMed1987

Dopaminergic regulation of fetal growth hormone (GH) secretion: study with maternal administration of bromocriptine.

To investigate the role of dopaminergic pathways on the control of growth hormone (GH) secretion, bromocriptine (BMC), a dopamine agonist drug, was orally administered at the dose of 5 mg to 46 pregnant women during labor whereas 41 received placebo. Maternal blood was obtained before drug administration and at delivery. Cord blood was obtained at delivery. Following the interval of time elapsed between BMC or placebo ingestion and parturition, maternal and cord blood samples were divided in 7 groups for statistical analysis. Cord blood GH resulted significantly higher than the corresponding maternal value (p less than 0.001). No significant change in GH values was observed nor in samples of mothers treated with BMC compared to mothers treated with placebo neither in cord blood samples of the corresponding neonates. These findings indicate that BMC administration does not modify GH secretion in the term fetus.

Bromocriptine↗
PubMed1987

Confirmation of the inhibitory influence of exogenous oxytocin on cortisol and ACTH in man: evidence of reproducibility.

The influence of low-dose oxytocin perfusion (32 mIU/min) on ACTH and cortisol plasma levels was tested in 8 normal male volunteers (age 18-26). The 1-h oxytocin perfusion periods were preceded and followed by two 1-h saline control periods. During the first period, there was a slight ACTH concentration decrease in 4 individuals. Oxytocin perfusion induced a clear-cut plasma ACTH decrease in 7 out of the volunteers, and a slight decrease in the remaining one. During the second saline infusion, there was a marked ACTH increase in 7 out of the volunteers, and a weak increase in one (P less than 0.0001). A similar pattern was observed in the plasma cortisol levels (P less than 0.00001). Furthermore, a control saline perfusion was performed in 4 of the 8 volunteers and compared to the 4 corresponding oxytocin perfusion tests: the differences between the 2 sets of tests was highly significant both for ACTH (P less than 0.003) and for cortisol (P less than 0.007). Lastly, the reproducibility of this inhibitory influence was retested in 4 volunteers: the tests were repeated under the same conditions 7 days later. There were no global differences between the 2 sets of tests either for ACTH (NS) or for cortisol (NS). ACTH and cortisol concentration fluctuations during the period between each set of tests were not significant. The following variations were measured for ACTH (NS) and for cortisol (NS). The present results confirm the inhibitory influence of low-dose oxytocin perfusion on ACTH and cortisol levels in normal males.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
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↗