Biomedical subjects

G Caffarri

Publications and source records attributed to G Caffarri.

At least 19 recordsLinked 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

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

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

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 effect of cigarette smoking on pituitary hormone secretions in insulin-dependent diabetes mellitus.

OBJECTIVE: We observed the effect of smoking two cigarettes on GH, AVP and cortisol secretion in patients with diabetes and normal subjects. DESIGN AND PATIENTS: We tested 10 male smokers with insulin-dependent diabetes mellitus (IDDM) and 10 normal smokers. On a different occasion, normal and diabetic smokers were tested with an insulin (0.15 U/kg body weight) tolerance test (ITT). MEASUREMENTS: Hypoglycaemia-induced hormonal responses in smokers were compared with those observed in 10 diabetic and 10 normal non smokers. RESULTS: All subjects showed similar basal GH, cortisol and AVP levels. In the normal subjects, cigarette smoking induced a significant increase in circulating GH, AVP and cortisol levels, with mean peaks 3.3, 3 and 1.58 times higher than baseline, respectively. Smoking-induced hormonal responses were significantly higher in diabetics (mean peak was 5.2 times higher than baseline for GH, 4.0 for AVP and 1.83 for cortisol). Insulin induced a similar hypoglycaemic nadir in all subjects at 30 minutes, even though the diabetic subjects had a delayed recovery in blood glucose levels. GH and AVP responses to hypoglycaemia were significantly higher in diabetic (mean peaks 11.5 and 3.2 times higher than baseline, respectively) than in normal (mean peaks 7.3 and 1.9) non-smokers, whereas these groups showed similar cortisol responses (mean peak 2.3 times higher than baseline). Smoking did not change any hypoglycaemia-induced hormonal rise in the normal controls, whereas it significantly enhanced GH, AVP and cortisol levels (mean peaks 14.5, 4 and 3.8 times higher than baseline, respectively) in diabetics. CONCLUSIONS: In patients with IDDM, cigarette smoking not only elicits higher GH, AVP and cortisol responses than in normal subjects, but also enhances the counter-regulatory hormone responses to insulin-induced hypoglycaemia. These findings suggest interactions between nicotine inhaled with cigarette smoking and diabetes-induced neuroendocrine alterations.

Adult↗

PubMed1997

Influence of residual C-peptide secretion on nocturnal serum TSH peak in well-controlled diabetic patients.

OBJECTIVE: Several alterations in hypothalamo-pituitary-thyroid (HPT) function have been described in diabetes mellitus and have been attributed to metabolic decompensation. The present study was performed in order to establish whether residual endogenous insulin secretion in patients with insulin-dependent diabetes mellitus (IDDM) may play a role in the control of HPT function. DESIGN: The nocturnal (2230 h-0200 h) serum TSH surge, the TSH response to TRH (200 microgram as an i.v. bolus) and serum free thyroid hormone levels were evaluated in C-peptide positive (CpP) (subjects with residual detectable endogenous pancreatic beta-cell activity) and C-peptide negative (CpN) patients both before and after optimization of metabolic status by 3 days of treatment with continuous subcutaneous insulin infusion, and in normal controls. TSH response to TRH and serum free thyroid hormone levels were assessed in the morning. SUBJECTS: Twenty male diabetic patients hospitalized to achieve a better control of hyperglycaemia were subdivided into 10 CpP (age: 33 +/- 1.5 years (mean +/- SE); body mass index (BMI): 22.6 +/- 0.3) and 10 CpN (age: 32 +/- 1.7 years; BMI: 22.5 +/- 0.4) patients. Nine normal men (age: 34.0 +/- 1.2 years; BMI: 23.1 +/- 0.4) served as controls. MEASUREMENTS: The nocturnal serum TSH peak was measured by dividing the highest night-time TSH value by the next morning TSH value and then multiplying by 100. Serum TSH levels were measured in samples taken just before (time 0) and 30 minutes, after TRH administration. Serum free thyroid hormone levels were measured in samples taken at time 0 of the TRH test. RESULTS: Before improvement of hyperglycaemia, CpP and CPN patients showed similar alterations in HPT function; i.e. serum free T3 levels and TSH responses to TRH were lower than normal; the nocturnal TSH surge was absent. Correction of hyperglycaemia normalized all examined HPT parameters in CpP diabetics, whereas normalization in serum free T3 levels and pituitary TSH responsiveness to TRH in CpN patients was not accompanied by restoration of the nocturnal TSH peak. CONCLUSIONS: These data indicate that the absence of residual pancreatic beta-cell function in patients with insulin-dependent diabetes mellitus is associated with neuroendocrine dysfunction in the regulation of circadian TSH secretion, which is not reversible after restoration of good glycaemic control.

Adult↗

PubMed1997

Involvement of nitric oxide in arginine, but not glucose, induced insulin secretion in normal men.

OBJECTIVE: At present, there are no reports in the literature of studies in humans concerning a possible role of nitric oxide (NO) in the regulation of pancreatic endocrine secretions, whereas studies in the rat provided discrepant results. The aim of this study was to clarify whether NO is involved in the control of insulin and/or glucagon secretion in basal conditions and/or in response to arginine or glucose administration in normal male subjects. DESIGN: We investigated whether an intravenous infusion of the NO synthase (NOS) inhibitor L-NAME, at a dose previously demonstrated not to produce blood pressure alterations or untoward side-effects, modifies insulin and/or glucagon secretory patterns. SUBJECTS: Fourteen healthy male volunteers aged 24-35 years, within 10-13% of their ideal body weight and without family history of diabetes mellitus or other endocrine diseases. METHODS: Seven normal men were treated intravenously with L-arginine (30 g in 50 ml of normal saline over 30 minutes) or glucose (0.33 g/kg body weight in a bolus) with or without the concomitant infusion of L-NAME (90 micrograms/kg in 50 ml of normal saline). L-NAME was infused for 30 minutes before and during arginine infusion and over 30 minutes before and 30 minutes after glucose injection. Another group of 7 men was infused over 60 minutes with L-NAME (90 micrograms/kg in 50 ml of normal saline) alone or saline alone. RESULTS: Basal and L-arginine or glucose induced glucagon secretions and basal and glucose stimulated insulin secretions were not altered by L-NAME administration. In contrast, the drug produced a partial but significant decrease in the insulin response to L-arginine. In fact, the mean peak insulin response to L-arginine was 5.3 times (53 +/- 5 mU/l (mean +/- SE)) higher than basal value (10 +/- 2) in the absence of L-NAME, but only 3.33 times (40 +/- 4) higher than baseline (12 +/- 3) during the infusion of the NOS-inhibitor. CONCLUSION: These data suggest that NO at least partially mediates the stimulatory action of L-arginine on insulin secretion in normal human subjects.

Adult↗

PubMed1997

Stimulation of arginine vasopressin secretion by a small increase in blood ionized calcium in normal men.

Evidence has been provided for an increase in baseline serum corticotrophin (ACTH) levels in response to a rise in circulating ionized calcium (Cai) levels within the physiological range. In order to establish whether small Cai increments are also able to modify the basal secretion of arginine vasopressin (AVP), we infused calcium gluconate through an intravenous infusion pump in eight healthy male subjects (25-31 years old). Serum Cai, ACTH and AVP concentrations were measured every 10 min over an infusion period lasting 90 min. A significant progressive rise in serum Cai (baseline: 42 +/- 0.9 mg dL-1; 90 min: 47.2 +/- 0.9 mg dL-1, P < 0.001), ACTH (baseline: 30.7 +/- 1.3 pg mL-1; mean peak at 80 min: 37.4 +/- 2.4 pg mL-1, P < 0.01) and AVP levels (baseline: 2.1 +/- 0.6 pg mL-1; mean peak at 80 min: 3.2 +/- 0.5 pg mL-1, P < 0.01) was observed during calcium infusion. Furthermore, a significant positive correlation (r = 0.71; P < 0.001) was observed between ACTH and AVP responses to calcium infusion at 60, 70, 80 and 90 min. These data demonstrate that AVP secretion is stimulated by a slight rapid increase in serum Cai levels even though absolute serum Cai levels remain within the normal range. In addition, the positive correlation between Cai-induced ACTH and AVP increments suggests that AVP plays a releasing role on ACTH secretion during calcium infusion.

Adrenocorticotropic Hormone↗

PubMed1997

Altered neuroendocrine control of GH secretion in normal women of advanced reproductive age.

BACKGROUND: Previous studies have suggested that the neuroendocrine control of growth hormone (GH) secretion changes with increasing age in women with normal menstrual cycles and sex steroid levels. METHODS: In order to verify this hypothesis, 8 younger (22-32 years) and 8 older (41-45 years) women with normal menstrual function and gonadal steroid levels were tested with the serotonergic agent sumatriptan (6 mg in a subcutaneous bolus), the GABAergic agonist sodium valproate (800 mg orally), the dopaminergic compound L-Dopa (500 mg orally) and placebos. Furthermore, all women were tested with GH-releasing hormone (GH-RH 1 microgram/kg body weight in an intravenous (i.v.) bolus) to determine whether GH secretion in response to its specific releasing factor was preserved. Serum GH levels were recorded over 2 hours in all tests and IGF-I levels in basal samples. RESULTS: Plasma IGF-I concentrations and the GH responses to sumatriptan, sodium valproate and L-Dopa were significantly lower in older than in younger women. Also, the GH-RH-induced GH response was significantly lower in older than in younger subjects. When peak GH responses to releasing stimuli were compared with age, significant negative correlations were found in all tests. CONCLUSIONS: These data did not show a specific neurotransmitter change underlying defective GH secretion in older aged reproductive women. On the other hand, the results indicated that age-related changes in the secretory machinery of GH, such as a reduced pituitary sensitivity to GH-RH and/or a reduction in the pituitary GH secretory capacity, affect women during the last years of the reproductive period.

Adult↗

PubMed1997

Age-related decrease in the opioid control of LH secretion during reproductive years in normal women.

UNLABELLED: Our previous studies showed that naloxone is unable to stimulate LH secretion in elderly men, suggesting a loss in the endogenous opioid inhibitory control of LH in senescence. METHODS: In the present study, we examined whether increasing age during the reproductive period in women is associated with alterations in the LH-releasing effect of naloxone. Studies were performed in younger (age 20-28 years, n = 8) and older (age 40-48 years, n = 8) subjects with normal menstrual cycles and normal gonadal steroid levels to avoid the interference of premenopause or menopause on gonadotropin secretion. The LH response to naloxone (4 mg as an i.v. bolus plus 10 mg infused in 2 h) was tested not only in normal conditions, but also after chronic dopaminergic stimulation with bromocriptine (5 mg/day for 7 days), because this treatment has been found able to restore normal LH responses to naloxone in elderly men. All tests were performed on the 22nd day of normal menstrual cycles. RESULTS: Naloxone induced a 100% increase in plasma LH levels in the younger group. In contrast, naloxone enhanced only by 50% LH secretion in the older subjects. When experiments were repeated after bromocriptine treatment, the effect of naloxone did not change in the younger subjects, whereas it was significantly higher in the older group. In the presence of bromocriptine, naloxone-induced LH increment in the older group was indistinguishable from that observed in the younger group. These data suggest that during the reproductive period, increasing age is associated with an impairment in the endogenous opioid control of LH secretion. In addition, age-related dopaminergic alterations independent of circulating gonadal steroid levels appear to underlie the defective endogenous opioid control of LH secretion in normally cycling women.

Adult↗

PubMed1996

Age-dependent decrease in the growth hormone response to growth hormone-releasing hormone in normally cycling women.

OBJECTIVE: To establish possible changes in GH secretion in normally cycling women with increasing age. DESIGN: Controlled clinical study. PATIENTS: Nine younger (18 to 33 years) and nine older (41 to 46 years) healthy women. SETTING: Tests were performed on the 22d day of regular cycles. INTERVENTION: All subjects were tested with GH-releasing hormone (GH-RH) (1 mg/kg body weight), the acetylcholinesterase inhibitor pyridostigmine (120 mg by mouth), the somatostatin inhibitor arginine (30 g infused IV over a 30-minute period) alone, and the combination of GH-RH plus arginine or GH-RH plus pyridostigmine. MAIN OUTCOME MEASURES: Glucose, cortisol, androgens, estrogens, thyroid hormones, and insulin growth-like factor (IGF-I) were measured in basal samples. Serum GH levels were measured in samples taken before and over a 2-hour period after drug administration. RESULTS: All basal hormonal values were similar in younger and older women. Insulin growth like factor-I levels were lower in older women. The GH responses to GH-RH alone, pyridostigmine alone, or the combination were lower in the older than in the younger group and were correlated negatively with age. In contrast, either arginine alone or GH-RH plus arginine produced similar GH responses in the two groups. CONCLUSION: These data indicate that the cholinergic stimulatory regulation of GH release is reduced in the older cycling women. Because acetylcholine inhibits hypothalamic somatostatin release, the reduced cholinergic tone in other subjects may result in an increased somatostatinergic tone. Normalization in older women of the reduced GH response to GH-RH by arginine supports this hypothesis.

Adolescent↗

PubMed1996

Influence of nitric oxide on hypoglycemia--or angiotensin II-stimulated ACTH and GH secretion in normal men.

In order to establish whether nitric oxide (NO) is involved in the regulation of ACTH and/or GH secretion, normal male subjects were treated i.v. with the NO-synthase (NOS) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) (40 micrograms/kg injected plus 50 micrograms/kg infused over 60 min) in basal conditions and/or during stimulation with insulin (0.15 IU/kg body weight in an i.v. bolus) to induce hypoglycemia (ITT) or ASP 1 ILE-5 angiotensin II (ANG II) (increasing doses of 4, 8 and 16 ng/kg/min, each dose for 20 min). The administration of L-NAME neither changed the basal secretion of ACTH and GH nor modified the hormonal responses to ANG II stimulation. Also the GH response during ITT remained unchanged in the presence of L-NAME. In contrast, the ACTH response to hypoglycemia was significantly higher when L-NAME was administered. These data suggest that in normal men NO has a negative effect on ACTH secretion, but not GH secretion, in response to hypoglycemia. Furthermore, our results argue against a role of NO in the control of basal and ANG II-stimulated ACTH and GH secretions.

Adrenocorticotropic Hormone↗

PubMed1996

Different effects of the serotonergic agonists buspirone and sumatriptan on the posterior pituitary hormonal responses to hypoglycemia in humans.

The responses of serum oxytocin (OT) and vasopressin (AVP) to the serotonergic HT1A agonist buspirone (15 mg p.o.) or the HTD1 agonist sumatriptan (6 mg injected subcutaneously) were evaluated in 7 normal men either in basal conditions or during an insulin (0.15 iu/kg as an i.v. bolus) tolerance test (ITT). Neither buspirone nor sumatriptan administration modified the basal secretion of AVP and OT. Stimulation of 5HT-1D receptors with sumatriptan was unable to change neither AVP nor OT response to insulin-induced hypoglycemia. On the other hand, the pretreatment with the 5HT1A agonist buspirone significantly enhanced the OT response during hypoglycemia, without modifying the AVP rise. The results of this study suggest that serotonergic 5HT1A receptors may interact with hypoglycemia in the stimulation of OT, but not AVP secretion.

Adult↗

PubMed1996

Effects of intravenously infused pituitary adenylate cyclase-activating polypeptide on adenohypophyseal Hormone secretion in normal men.

The possible stimulatory effects of an intravenous infusion of increasing amounts of pituitary adenylate cyclase-activating polypeptide (PACAP) on anterior pituitary hormone secretions were evaluated in humans. Successively increasing doses of PACAP-38 (2, 4 and 8 pmol.kg-1.min-1; each dose for 20 min) were infused i.v. in 7 normal male subjects. On a different occasion, the same subjects were tested with vasoactive intestinal peptide (VIP; 4 pmol.kg-1.min-1 for 60 min). Circulating GH, ACTH, PRL, TSH and gonadotropin concentrations were measured before PACAP infusion and every 20 min, just before increasing the infusion dose of PACAP. Blood samples were taken before and every 15 min after the beginning of VIP administration. Serum levels of GH, TSH and gonadotropins did not change during PACAP or VIP infusion. Circulating ACTH and PRL concentrations were not modified by the infusion of the lowest dose of PACAP, whereas they were significantly increased in a dose-response fashion when higher amounts of PACAP were given. PRL, but not ACTH levels were significantly increased by VIP infusion. These data show for the first time in humans that ACTH and PRL secretions from the anterior pituitary gland are stimulated by the systemic administration of PACAP. In addition, since VIP stimulated only PRL secretion, PACAP-induced ACTH release appears to be mediated by specific receptors.

Adult↗