Biomedical subjects

V Coiro

Publications and source records attributed to V Coiro.

At least 37 records · Page 2Linked to original sources

PubMed1998

Stimulation of ACTH and GH release by angiotensin II in normal men is mediated by the AT1 receptor subtype.

This study was performed in order to determine whether the stimulatory effect of plasma angiotensin II (ANG II) on Adrenocorticotropic hormone (ACTH) and growth hormone (GH) secretion in humans is mediated by AT1 subtype receptors. For this purpose, the effects of the administration of the AT1 receptor antagonist, losartan (50 mg p.o.) or a placebo on the ACTH and GH responses to ANG II (i.v. infusion for 60 min of successively increasing doses (4, 8 and 16 ng/kg/min); each dose for 20 min) were evaluated in eight normal men. ANG II infusion induced significant increases in both serum ACTH and GH levels (mean peaks were 1.6- and four-times higher than baseline, respectively). The ACTH response to ANG II was completely abolished by pretreatment with losartan. Also, the ANG II-induced GH rise was reduced by administration of losartan, but the GH response was still significantly higher than the basal value (mean peak was twice as high as the baseline). These data provide evidence of AT1 receptor involvement in mediation of the ANG-II stimulating effect on ACTH and GH secretion.

Adrenocorticotropic Hormone↗

PubMed1998

5-HT3 serotonergic receptor mediation of hypoglycemia-induced arginine-vasopressin but not oxytocin secretion in normal men.

The present study was undertaken in order to establish the possible involvement of 5-HT3 serotonergic receptors in the control of basal and/or hypoglycemia-stimulated arginine vasopressin (AVP) and/or oxytocin (OT) secretion. For this purpose, 12 normal men were injected intravenously with a bolus of 4 mg ondansetron, a specific 5-HT3 receptor antagonist, under basal conditions (n = 6) or 30 min before insulin (0.15 IU/kg body weight) administration (n = 6) (insulin tolerance test (ITT)). Control experiments with normal saline instead of ondansetron treatment were performed. Furthermore, on a different occasion, the same subjects were tested in identical experimental conditions with 8 mg ondansetron. Our results showed that the hypoglycemic response to insulin was similar during the ITT and ondansetron plus ITT. Inhibition of 5-HT3 serotonergic receptors with ondansetron (4 or 8 mg) did not modify the basal secretion of AVP and OT and the OT response to insulin-induced hypoglycemia. In contrast, the administration of 4 or 8 mg ondansetron significantly reduced in a similar manner hypoglycemia-induced AVP rise. Mean peak level at 45 min after insulin injection was 2.25 times higher than baseline in the control ITT and 1.5 times higher than basal value in the ondansetron (4 or 8 mg) plus ITT. These data demonstrate that 5-HT3 serotonergic receptors at least partially mediate the AVP response to hypoglycemia, without modifying the simultaneous OT response. On the other hand, 5-HT3 receptors do not appear to be involved in the control of basal posterior pituitary hormone secretions.

Adult↗

PubMed1998

Melatonin inhibits oxytocin response to insulin-induced hypoglycemia, but not to angiotensin II in normal men.

In order to establish whether melatonin alters basal and/or stimulated oxytocin secretion, 18 normal men were treated (p.o.) with 6 or 12 mg melatonin or placebo in basal conditions (N-6 subjects) or concomitantly to the administration of insulin (O.15 IU/kg body weight in an i.v. bolus) (N-6 subjects) or angiotensin II (increasing doses of 4, 8 and 16 ng/kg/min, at intervals of 20 min). The administration of 6 or 12 mg melatonin did not change basal and angiotensin II-stimulated oxytocin secretion. In contrast, the oxytocin response to insulin-induced hypoglycemia was significantly reduced by melatonin treatment. In fact, the mean peak oxytocin response to hypoglycemia was 2.2 times higher than baseline in the absence of melatonin, whereas it was 1.6 times higher than basal value after administration of 6 or 12 mg melatonin. These data indicate an involvement of melatonin in the regulation of the oxytocin response to hypoglycemia in normal men. The lack of effects of melatonin on basal and angiotensin II-stimulated oxytocin secretion argues against the possibility that melatonin exerts an overall modulatory role on oxytocin secretion in humans.

Adult↗

PubMed1998

Oxytocin enhances the prolactin response to vasoactive intestinal polypeptide in healthy women.

OBJECTIVE: To establish whether oxytocin modifies the stimulatory effect of vasoactive intestinal polypeptide (VIP) on prolactin secretion in healthy women. DESIGN: Controlled clinical study. SETTING: Healthy women in an academic research environment. PATIENT(S): Seven healthy women (aged 24-32 years) were tested on the 22nd day of two consecutive normal menstrual cycles. INTERVENTION(S): Vasoactive intestinal polypeptide (4 pmol x kg(-1) x min(-1) in 50 mL of normal saline infused i.v. for 60 minutes) was administered in either the presence or absence of concurrent treatment with oxytocin (2 IU injected plus 0.07 IU/min infused for 60 minutes). MAIN OUTCOME MEASURE(S): Serum prolactin levels. RESULT(S): The administration of VIP induced a significant increase in serum prolactin levels, with a mean peak response 1.6 times higher than baseline at 45 minutes after injection. In the presence of oxytocin, the prolactin response to VIP was significantly higher, with a mean peak response 2 times higher than baseline. CONCLUSION(S): These data suggest that in healthy women, oxytocin facilitates the regulation of the stimulating effect of VIP on prolactin secretion.

Adult↗

PubMed1998

Different effects of naloxone on the growth hormone response to melatonin and pyridostigmine in normal men.

The effect of melatonin (MEL) (12 mg orally), pyridostigmine (60 mg orally), the combination of MEL and pyridostigmine, or placebo on growth hormone (GH) secretion was tested in seven normal men. In addition, MEL tests and pyridostigmine tests were repeated after pretreatment with naloxone (1.2-mg bolus followed by intravenous [i.v.] infusion of 1.6 mg/h for 3 hours). Serum GH levels increased fivefold after MEL and sixfold after pyridostigmine administration. The concomitant administration of MEL did not change the GH response to pyridostigmine. In the presence of naloxone, the GH response to MEL was completely abolished, whereas naloxone did not modify the pyridostigmine-induced GH increase. These data suggest that MEL and pyridostigmine stimulate GH secretion through a common mechanism, which is probably represented by the inhibition of somatostatin activity. However, in contrast to pyridostigmine, the action of MEL appears to be exerted through a naloxone-sensitive opioid mediation.

Administration, Oral↗

PubMed1998

Different effects of pyridostigmine on the thyrotropin response to thyrotropin-releasing hormone in endogenous depression and subclinical thyrotoxicosis.

Primary organic disorders of the thyroid gland must be excluded in interpreting the thyrotropin (TSH)-releasing hormone (TRH) test in affective disease. Both endogenous depression and subclinical thyrotoxicosis are frequently associated with low basal TSH levels and a blunted (<5 mIU/L) TSH response to TRH despite thyroid hormone levels within the normal range. The present study was performed to establish whether a reduction of the hypothalamic somatostatinergic tone by treatment with the acetylcholinesterase inhibitor pyridostigmine before TRH might be useful to distinguish endocrine from affective diseases. Twelve male depressed patients (aged 41.4 +/- 3.1 years) and 12 men (aged 43.4 +/- 4.1 years) with subclinical thyrotoxicosis because of autonomous thyroid nodules were selected according to the presence of a low basal TSH level and a blunted TSH response to 200 microg TRH intravenously (IV) (TSH increment was <5 mIU/L at 30 minutes [peak] after TRH) but thyroid hormone levels within the normal range. All patients were tested again with TRH 60 minutes after treatment with 180 mg pyridostigmine orally. Eleven normal men served as controls. Basal TSH levels were 0.2 +/- 0.2 mIU/L (mean +/- SE) in depression and 0.1 +/- 0.2 in subclinical thyrotoxicosis (normal controls, 1.4 +/- 0.3). In both groups, the mean peak response to TRH was significantly higher than baseline; however, according to selection, the TSH increase was less than 5 mIU/L. Pyridostigmine did not change basal TSH levels in any group, but significantly enhanced the TRH-induced TSH increase in normal controls and in depressed subjects (TSH increment became >7 mIU/L in all depressed subjects). In contrast, no significant change in the TSH response to TRH was observed in subclinical thyrotoxicosis after pyridostigmine treatment. Basal and TRH- and pyridostigmine + TRH-induced TSH levels were significantly higher in the normal controls than in the other groups. These data show a cholinergic involvement in the blunted TSH response to TRH in patients with endogenous depression, but not in subjects with subclinical thyrotoxicosis, suggesting that these diseases could be separated on the basis of the pyridostigmine + TRH-induced TSH response test.

Adult↗

PubMed1998

Arginine vasopressin and oxytocin responses to angiotensin II are mediated by AT1 receptor subtype in normal men.

This study was performed to determine whether the stimulatory effect of plasma angiotensin II (ANG II) on arginine vasopressin (AVP) and oxytocin (OT) secretion in humans is mediated by AT1 subtype receptors. For this purpose, the effects of the AT1 receptor antagonist losartan (50 mg orally) or a placebo on the AVP and OT responses to ANG II (intravenous infusion for 60 minutes of successively increasing doses of 4, 8, and 16 ng/kg min; each dose for 20 minutes) administration were evaluated in seven normal men. In additional experiments, the same subjects were tested with losartan (50 mg orally) alone or placebo alone. Neither losartan nor placebo given alone modified the basal levels of AVP and OT. ANG II infusion induced significant increments in both serum AVP and OT levels (mean peaks were 1.55 and 1.41 times higher than baseline, respectively). Both hormonal responses to ANG II were completely abolished by pretreatment with losartan. These data provide evidence of AT1 receptor involvement in mediation of the ANG II-stimulating effect on AVP and OT secretion.

Adult↗

PubMed1998

Involvement of nitric oxide in vasoactive intestinal peptide-stimulated prolactin secretion in normal men.

To establish whether nitric-oxide (NO) participates in the regulation of prolactin (PRL) secretion in humans in basal conditions and/or under stimulation with vasoactive intestinal polypeptide (VIP), seven normal men were treated with a placebo (normal saline) or the NO synthase (NOS) inhibitor L-NAME (40 microg/kg injected plus 50 microg/kg infused intravenously over 60 minutes), which in previous studies has been found able to modify other pituitary hormone secretions. Experiments were performed either in basal conditions or during stimulation of PRL secretion with an intravenous infusion of VIP (4 pmol/kg min over 60 minutes). The administration of L-NAME was unable to change the basal secretion of PRL. In contrast, L-NAME significantly enhanced the PRL increase induced by VIP. These data argue against an involvement of NO in regulation of basal PRL secretion. In contrast, the stimulatory effect of L-NAME on VIP-induced PRL secretion suggests that NO exerts an inhibitory control of the PRL response to VIP.

Adult↗

PubMed1998

Effect of melatonin on arginine vasopressin secretion stimulated by physical exercise or angiotensin II in normal men.

The present study was undertaken in order to establish the possible involvement of melatonin in the mechanisms underlying the arginine-vasopressin (AVP) responses to physical exercise and angiotensin II (ANG II). On two mornings at least 1 week apart, normal male subjects were tested with exercise on a bicycle ergometer (the workload was gradually increased at 3-min intervals until exhaustion and lasted about 15 min in all subjects) or ANG II (60-min infusion of ANG II (Asp 1, IIe 5 angiotensin II) dissolved in 5% glucose in successively increasing doses of 4, 8, 16 ng/kg/min; each dose for 20 min). Tests were carried out with the administration of either 6 mg melatonin or placebo. Melatonin treatment neither modified the basal concentrations of AVP nor changed the AVP response to ANG II. In contrast, plasma AVP levels rose 3.6 times during exercise in the absence of melatonin, but only 2.3 times in the presence of melatonin. These data indicate an involvement of melatonin in the mechanism underlying the AVP response to physical exercise, but not ANG II, in normal men.

Adult↗

PubMed1998

Alcoholism abolishes the effects of melatonin on growth hormone secretion in humans.

Chronic alcohol consumption profoundly affects hypothalamic-pituitary function. The present study was performed in order to establish whether alcoholism modifies the effects of melatonin (MEL) on the neuroendocrine control of growth hormone (GH) secretion. For this purpose, the effects of oral administration of 12 mg MEL or placebo on basal and hypoglycemia-stimulated GH secretion were tested in nine (40-52-year-old) alcoholic men after 10-31 days of abstinence and in nine age- and weight-matched normal controls. Hypoglycemia was induced with an intravenous bolus injection of 0.15 IU/kg body weight of insulin. MEL but not placebo administration induced a small, but significant increase in basal GH secretion in the normal controls. In contrast, neither MEL nor placebo treatment significantly changed the basal serum GH levels in alcoholic men. Both groups showed a similar hypoglycemic pattern after insulin administration. The GH response to insulin-induced hypoglycemia was significantly lower in alcoholic than in normal subjects. MEL administration significantly reduced hypoglycemia-induced GH rise in the normal controls, but not in alcoholic patients. These data show that alcoholism not only reduces the GH response to insulin-induced hypoglycemia, but also abolishes MEL actions on basal and hypoglycemia-stimulated GH secretion.

Adult↗

PubMed1998

Effect of nitric oxide on basal and TRH-or metoclopramide-stimulated prolactin release in normal men. volpi@ipruniv.cce.unipr.it.

In order to establish whether nitric oxide (NO) is involved in the regulation of basal and/or TRH- or metoclopramide (MCP)-stimulated PRL secretion, normal male subjects were treated i.v. with the NO-synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME) (40 mg/kg injected plus 50 mg/kg infused over 60 min) in basal conditions (N.7 subjects) or just before the PRL releasing hormone TRH (20 or 200 microg iv) (N.7 subjects) or the antidopaminergic agent MCP (1 or 10 mg iv) (N.7 subjects). In control experiments, subjects received normal saline instead of L-NAME. The administration of L-NAME modified neither the basal secretion of PRL, nor the PRL release induced by TRH (20 or 200 microg) or MCP (1 or 10 mg). These data suggest that in humans, NO is not involved in the control of PRL release at the anterior pituitary level.

Adult↗

PubMed1998

Alcoholism abolishes the gamma-aminobutyric acid (GABA)ergic control of GH secretion in humans.

In order to establish possible alterations in the gamma-aminobutyric acid (GABA)ergic control of growth hormone (GH) secretion in alcoholics, 800 mg sodium valproate (a drug enhancing endogenous GABA activity), 10 mg baclofen (a GABA(B) receptor agonist) or a placebo were given orally to nine normal men (age 38-48 years) and nine 2-4-week-abstinent alcoholics (age 35-50 years; duration of alcohol consumption 3-6 years). Blood samples for GH assay were taken every 30 min for the next 150 min. Both drugs induced a significant increment in serum GH levels in the normal controls; mean peak was 7.2 and 3.27 times higher than baseline after sodium valproate and baclofen, respectively. In contrast, GH secretion in alcoholic patients did not change after baclofen or sodium valproate administration. Placebo administration did not modify GH secretion in any subject. In concurrence with previous reports showing alterations of GABAergic neurotransmission in the central nervous system of patients affected by alcoholism, these data show the loss of the GABAergic mechanism(s) underlying the GH response to sodium valproate and/or baclofen action in alcoholism.

Adult↗

PubMed1998

Influence of residual insulin secretion and duration of diabetes mellitus on the control of luteinizing hormone secretion in women.

BACKGROUND: The aim of the present study was to establish whether the persistence of residual beta-cell activity after long-term diabetes mellitus (DM) exerts a protective role on luteinizing hormone (LH) secretion. METHODS: The LH responses to stimulation with gonadotropin-releasing hormone (Gn-RH) (100 microg in an i.v. bolus) or naloxone (4 mg injected in an i.v. bolus, followed by the constant infusion of 8 mg in 2 h) were measured in C-peptide-positive (CpP) and C-peptide-negative (CpN) normally menstruating women with short-term (group 1 < 3 years, CpP n = 11, CpN n = 11) or long-term (group 2 > 10 years, CpP n = 11, CpN n = 11) DM and in age-matched normal control subjects (n = 11). RESULTS: Gn-RH induced significant increments in LH secretion in all groups. Significant LH responses to naloxone were observed in all groups, except in group 2 CpN patients. However, the LH response to either Gn-RH or naloxone was significantly lower in group 1 CpN, group 2 CpP and group 2 CpN patients than in the normal control subjects. Furthermore, the LH response was significantly lower in group 2 CpP than in group 1 CpP patients and in group 2 CpN than in group 1 CpN subjects. CONCLUSIONS: These results indicate a role for both deficiency in residual endogenous insulin secretion and duration of diabetes in the derangement of LH secretory control. The data suggest that the protective role exerted by residual beta-cell activity on LH secretion during the early years of DM diminishes with time elapsed after the onset of diabetes mellitus.

Adult↗

PubMed1998

Effect of residual endogenous insulin secretion on the abnormal oxytocin response to hypoglycaemia in insulin-dependent diabetics.

OBJECTIVES: Arginine-vasopressin (AVP) and oxytocin (OT) secretions are abnormally stimulated by hypoglycaemia in patients with IDDM. Since previous studies showed that AVP secretion is influenced by the persistence of residual endogenous insulin secretion, we wondered whether this factor also regulates OT secretion. DESIGN: Case-control study: the OT response to insulin-induced hypoglycaemia was measured in normal and diabetic patients with or without residual endogenous insulin secretion. SUBJECTS: Ten normal male subjects, 10 C-peptide positive (CpP) and 11 C-peptide negative (CpN) male diabetic patients. TESTS PRELIMINARY STUDIES: plasma C-peptide levels were measured after intravenous administration of 1 mg glucagon. Insulin tolerance test (ITT): diabetics were studied after optimization of their metabolic status by 3 days of treatment with constant subcutaneous insulin infusion. CpP and CpN diabetics and normal controls were tested with an intravenous administration of 0.15 IU per kg body weight insulin. Blood samples for OT assay were taken just before the rapid injection of insulin (time 0) and at time 15, 30, 45 and 60 min. RESULTS: The basal concentrations of OT were similar in all groups. Insulin induced a similar hypoglycaemic nadir in all groups at 30 min, even though diabetic groups showed a delayed recovery in blood glucose levels. The glycaemic pattern was similar in all diabetic patients. Hypoglycaemia-induced OT rise was significantly higher in the two diabetic groups than in the normal group. However, CpN patients showed significantly higher OT increments than CpP subjects. CONCLUSIONS: These data indicate that a residual endogenous insulin secretion exerts a partial protective action against the hypothalamic-pituitary disorder affecting the OT secretory system in IDDM.

Adult↗

PubMed1997

Beta-endorphin, adrenocorticotropic hormone and cortisol secretion in abstinent alcoholics.

The circadian secretion of beta-endorphin, adrenocorticotropic hormone (ACTH), and cortisol was evaluated in 14 non-cirrhotic alcoholic men after 7 and 28 days of abstinence and in 12 sex- and age-matched normal subjects. A significant decrease in plasma levels of beta-endorphin, reduced ACTH levels, and increased cortisol levels were observed in samples taken at 08.00 h, 12.00 h, 18.00 h, and 23.00 h both after 7 and 28 days of abstinence. These data suggest the presence of a strong negative feedback on pro-opiomelanocortin synthesis by cortisol hypersecretion in abstinent alcoholics, which might be due to long-term stimulation of adrenal function by alcohol. The decreased plasma beta-endorphin levels might predispose to relapse in alcohol abuse.

Adrenocorticotropic Hormone↗

PubMed1997

Effects of thyrotropin-releasing hormone and metoclopramide on PRL secretion in normally cycling and amenorrheic alcoholic women.

To assess the possible influence of alcoholism on the dopaminergic inhibitory control of prolactin (PRL) secretion, 10 mg of the dopaminergic antagonist metoclopramide (MTC), was injected i.v. in a group of eight healthy abstemious women (aged 28 +/- 6 (mean +/- S.E.) years) and in 16 aged-matched nondepressed female alcoholic subjects after 3-4 weeks of abstinence from alcohol. All normal controls and eight alcoholics had normal menstrual cycles and were tested in the early follicular phase (4-8 days), the remaining eight alcoholics were affected by amenorrhea (duration: 15 +/- 3 months). During the same period, all patients were also tested with TRH (200 micrograms in an i.v. bolus) to determine whether the pituitary PRL cell secretory capacity was preserved in alcoholics. The amenorrheic alcoholic group showed strikingly lower circulating estrogen levels than normally cycling groups. Similar basal PRL levels and PRL responses to TRH were observed in normal controls and normally cycling alcoholics, whereas basal and TRH-stimulated PRL levels were significantly higher in amenorrheic alcoholics. In contrast, the PRL response to MTC was significantly higher in cycling alcoholic patients than in normal controls and amenorrheic alcoholic subjects. However, when the statistical analysis of MTC test took into account the difference in estrogen levels among groups, the statistical differences in the PRL responses to MTC observed between normally cycling and amenorrheic alcoholics disappeared. These data suggest the presence of an enhanced dopaminergic inhibitory control of PRL secretion in 2-3 week abstinent alcoholics with normal menstrual cycles and normal circulating estrogen levels. In contrast, amenorrhea in abstinent alcoholics appears to be associated with an enhancement of PRL cell secretory activity.

Adult↗

PubMed1997

Effect of melatonin on hypoglycemia and metoclopramide-stimulated arginine vasopressin secretion in normal men.

The present study was performed in order to establish whether melatonin (MEL) plays a role in the regulation of arginine vasopressin secretion (AVP) in normal human subjects. For this purpose, the effects of an oral administration of 6 or 12 mg MEL on basal and metoclopramide (MCP)- or hypoglycemia-stimulated AVP secretion was tested in 18 normal men. MCP was given at a dose of 20 mg as an intravenous (i.v.) bolus; hypoglycemia was induced with an i.v. bolus injection of 0.15 IU/kg body weight of insulin. In addition, in view of the well-known inhibitory effect of MEL on the growth hormone (GH) response to hypoglycemia, GH levels were measured during the insulin tolerance test (ITT), as an independent index of MEL activity. MEL did not produce any change in AVP secretory patterns in basal conditions or during the MCP test. In contrast, the mean peak AVP response to hypoglycemia was 2.33 times higher than baseline in the control ITT, whereas it was only 1.77 times higher than baseline in the ITT plus MEL tests. Also, the GH response to hypoglycemia was significantly lower in the presence than in the absence of MEL. For both AVP and GH, the inhibitory effect of MEL during ITT was similar, when either 6 or 12 mg MEL was given. These data indicate an involvement of MEL in the control of the AVP response to hypoglycemia, but not of basal and MCP-induced AVP secretion. In addition, the similar effects of MEL on GH and AVP secretions during ITT suggest that similar neuroendocrine mechanisms underlie these hormonal responses to hypoglycemia.

Administration, Oral↗

PubMed1997

Abnormal plasma oxytocin and beta-endorphin levels in alcoholics after short and long term abstinence.

1. Plasma oxytocin (OX), vasopressin (VP), estrone (ES) and beta-endorphin (beta-end) levels were measured in 13 male non-chirrotic alcoholics, at 1, 4, 7, 15 and 28 days after alcohol withdrawal and only once in 9 sex- and age-matched normal controls. 2. At all examined time points, plasma OX and ES, but not VP, levels were significantly higher in alcoholics than in controls. Alcoholics showed plasma beta-end levels lower than normal. 3. A positive relationship was found between ES and OX levels suggesting that elevated estrogens levels in chronic alcoholics might exert a stimulatory effect on OX. 4. In light of the well-known effect of OX on learning and memory, an involvement of OX in alcohol-induced neuropsychological deficits may be supposed.

Adult↗