Biomedical subjects

L Capretti

Publications and source records attributed to L Capretti.

At least 37 records · Page 2Linked to original sources

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↗

PubMed1996

Gamma-aminobutyric acid mediation of the inhibitory effect of nitric oxide on the arginine vasopressin and oxytocin responses to insulin-induced hypoglycemia.

Previous studies have demonstrated that the nitric oxide (NO) synthase inhibitor L-NAME exerts positive effects on the arginine vasopressin (AVP) and oxytocin (OT) responses to insulin-induced hypoglycemia, suggesting inhibitory actions of NO. The present study was designed to determine whether a gamma-aminobutyric acid (GABA)ergic pathway is involved in regulation of NO action. AVP and OT secretory patterns during insulin (0.15 IU/kg, i.v.)-tolerance tests (ITT) were examined in seven normal male subjects with (experimental tests) and without (control test) concomitant treatment with L-NAME (40 micrograms/kg injected plus 50 micrograms/kg infused, i.v.), the GABAergic agent sodium valproate (600 mg in three divided doses orally) or the combination of L-NAME and sodium valproate. Insulin-induced hypoglycemia increased by 2-fold (peak vs. baseline) plasma AVP and OT levels. In the presence of L-NAME, plasma AVP and OT levels rose 3-fold in response to hypoglycemia and were significantly higher than those in the control test. Administration of sodium valproate alone changed neither AVP nor OT secretory patterns during ITT. In contrast, sodium valproate abolished the facilitating effect of L-NAME on both AVP and OT responses to hypoglycemia. In the ITT plus L-NAME plus sodium valproate test, plasma AVP and OT levels were not significantly different at any time point from those observed during the control ITT. These data indicate a GABAergic mediation of the inhibitory modulation by NO of the AVP and OT responses to insulin-induced hypoglycemia.

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↗

PubMed1996

Inhibition by somatostatin of the growth hormone, but not corticotropin response to angiotensin II in normal men.

The effect of an i.v. infusion of somatostatin (SRIH) (4.1 micrograms/min/180 min) on angiotensin II (ANG II infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg/min; each dose for 20 min)-stimulated growth hormone (GH) and corticotropin (ACTH) release was studied in 7 normal men. In addition, 7 additional normal subjects were tested with ANG II alone (as described above), GH-RH (0.1 microgram/kg body weight as an i.v. bolus) alone or the combination of GH-RH and ANG II. The ACTH response to ANG II was not modified by SRIH infusion; in contrast, the GH response to ANG II was significantly reduced by the concomitant treatment with SRIH. On the other hand, the administration of GH-RH together with ANG II produced peak GH levels comparable to the sum of the individual responses to ANG II and GH-RH, given alone. These findings provide evidence that the stimulatory effect of ANG II on GH, but not ACTH secretion, is under the inhibitory control of somatostatin, suggesting an interaction between ANG II and SRIH in regulation of GH secretion.

Adrenocorticotropic Hormone↗

PubMed1995

Effects of intravenously infused pituitary adenylate cyclase-activating polypeptide on arginine vasopressin and oxytocin secretion in man.

In order to establish possible stimulatory effects of increasing plasma concentrations of pituitary adenylate cyclase-activating polypeptide (PACAP) on arginine vasopressin (AVP) and/or oxytocin (OT) secretion, successively increasing doses of PACAP-38 (2, 4 and 8 pmol kg min-1; each dose for 20 min) were infused in seven normal men. Plasma AVP and OT levels were measured before infusion and every 20 min, just before increasing the infusion dose of PACAP. During tests, PACAP infusion did not produce untoward side effects or changes in blood osmolality and/or pressure. Plasma OT levels did not change during PACAP infusion. Plasma AVP concentrations were not modified by infusion of the lowest dose of PACAP, whereas they were significantly increased in a dose-response fashion when higher amounts of PACAP were given. These findings demonstrate for the first time in humans that the systemic administration of PACAP exerts stimulatory effects on AVP, but not OT secretion.

Adult↗

PubMed1995

Effect of substance P on basal and thyrotropin-releasing hormone-stimulated thyrotropin release in humans.

To test the possible effects of intravenous administration of substance P (SP) on basal and thyrotropin-releasing hormone (TRH)-stimulated thyrotropin (TSH) release, SP was infused alone (0.5 or 1.5 pmol/kg-1/min-1 for 60 minutes) or after TRH (20 or 400 micrograms in an intravenous bolus) in 21 normal male subjects (aged 26 to 36 years) and in 18 normal women (aged 25 to 32 years). Women were studied during follicular (day 6 to 8) and luteal (day 21 to 23) phases of following regular menstrual cycles. In addition, plasma cortisol levels during SP infusion were measured. In agreement with previous findings, significant increments in plasma cortisol levels were observed in men and women when the higher (1.5 pmol/kg-1/min-1) but not the lower (0.5 pmol/kg-1/min-1) amount of SP was administered. In contrast, in both men and women basal and TRH (20 or 400 mg)-induced TSH releases were not modified by SP at any tested amount. Results in the follicular and luteal phase were similar. These data suggest that in normal men and women plasma SP is not involved in the control of TSH release, at least not outside the blood-brain barrier.

Adult↗

PubMed1995

Low-dose ovine corticotropin-releasing hormone stimulation test in diabetes mellitus with or without neuropathy.

The function of the hypothalamic-pituitary-adrenal (HPA) axis was evaluated in insulin-dependent diabetics without (group I, n = 10) or with (group II, n = 10) established symptomatic neuropathy and in age- and weight-matched normal controls (n = 11). Since the corticotropin (ACTH)/cortisol response to the minimal-effective dose of corticotropin-releasing hormone ([CRH] 0.03 microgram/kg body weight) represents a useful tool for HPA axis examination, all subjects were tested with the low-dose ovine CRH stimulation test. Experiments started at 8:30 AM, when CRH was injected after two basal blood samples were withdrawn, and lasted 2 hours. Basal serum levels of ACTH were similar in the three groups. Administration of CRH induced a small but significant increase in ACTH levels in all subjects; however, the CRH-induced ACTH increase was significantly higher in normal controls than in diabetic groups I and II. Furthermore, a significantly lower ACTH response was observed in group II than in group I. In contrast, basal and CRH-induced cortisol levels were significantly higher in diabetics than in normal controls. Comparisons between diabetic groups showed that both basal and stimulated cortisol secretion was significantly higher in group II than in group I. When peak ACTH responses to CRH and basal cortisol levels were combined, a significant negative correlation was found (r = .545, P < .02). These data show that even uncomplicated diabetes mellitus is associated with adrenal hyperfunction. Such an alteration is more pronounced in the presence of neuropathy.

Adrenocorticotropic Hormone↗

PubMed1995

Mediation by nitric oxide of LH-RH-stimulated gonadotropin secretions in human subjects.

In order to establish whether nitric-oxide (NO) participates in the regulation of gonadotropin secretion in humans, seven normal men were treated with a placebo (normal saline) or the NO synthase inhibitor L-NAME, given at doses (40 micrograms/kg injected plus 50 micrograms/kg infused i.v.) previously found to be unable to change blood pressure. Experiments were carried out either in basal conditions or during stimulation of gonadotropin secretion with an intravenous injection of 100 micrograms LH-RH. The administration of L-NAME was unable to change the basal secretion of FSH and LH. In contrast, L-NAME significantly reduced both FSH and LH increments induced by LH-RH. These data fail to provide evidence of NO involvement in regulation of basal gonadotropin secretion. In contrast, the inhibitory effect of L-NAME on LH-RH-induced LH and FSH secretion suggests the modulation by NO of the gonadotropin releasing action of LH-RH.

Adult↗

PubMed1995

Dopaminergic and cholinergic control of arginine-vasopressin secretion in type I diabetic men.

Enhanced cholinergic and dopaminergic controls of anterior pituitary function have been described in insulin-dependent diabetes mellitus (IDDM). In order to verify whether similar neurotransmitter alterations also affect the regulation of posterior pituitary hormone secretion, the arginine-vasopressin (AVP) responses to the dopaminergic agonist apomorphine and in a different occasion to physostigmine, an acetylcholinesterase inhibitor, were evaluated in normal (n = 10) and type I diabetics (n = 16). In addition, a control test with normal saline was performed in all subjects. None of the diabetic patients were affected by neuropathy or other diabetic complications. They were divided into two groups according to the duration of their disease (less than 10 years: group 1, n = 8; more than 10 years: group 2, n = 8). Physostigmine (12.5 micrograms kg-1) was infused intravenously over 10 min; apomorphine (60 micrograms kg-1) was injected subcutaneously. Basal AVP concentrations were similar in all groups and remained constant during the control test. In contrast, both drugs induced significant increments in plasma AVP levels in the normal controls and diabetic subjects. However, physostigmine- and apomorphine-induced AVP increments were twofold higher in diabetics than in control subjects. No significant differences were observed between diabetics of groups 1 and 2. No significant correlations between duration of diabetes and peak AVP responses to physostigmine or apomorphine were found within each group or when all diabetic subjects were considered together. These data indicate enhancement of both dopaminergic and cholinergic stimulatory regulations of AVP secretion in patients with uncomplicated IDDM, regardless of the duration of diabetes.

Acetylcholine↗

PubMed1995

Influence of residual C-peptide secretion on the arginine vasopressin response to hypoglycaemia and metoclopramide in insulin-dependent diabetes.

Arginine vasopressin (AVP) hypersecretion in response to metoclopramide or to insulin-induced hypoglycaemia has been described in type I diabetes mellitus. In the present study, we examined whether residual endogenous insulin secretion may play a role in the control of this abnormal AVP secretory pattern. For this purpose, 21 insulin-dependent diabetic men and 10 age- and weight-matched normal men were tested with MCP (20 mg in an i.v. bolus). On a different occasion, subjects were tested with insulin (0.15 IU kg-1). The diabetic patients were subdivided into C-peptide negative patients (CpN, 11 patients without detectable endogenous pancreatic beta cell activity) (group I) and C-peptide positive patients (CpP, 10 patients with residual endogenous insulin secretion) (group II). Experiments started after optimization of the metabolic status of the diabetic men by 3 days of treatment with continuous subcutaneous insulin infusion. The basal concentrations of AVP were similar in all groups. The administration of MCP induced a striking elevation in plasma AVP levels in the normal controls and in the diabetic subjects of groups I and II. However, the AVP rise was significantly higher in group I and group II than in normal controls. Furthermore, group I diabetics showed higher AVP increments than group II. Insulin induced a similar hypoglycaemic nadir in all subjects at 30 min, even though the diabetic subjects of groups I and II had a delayed recovery in blood glucose levels. The hypoglycaemic pattern was similar in group I and II. Hypoglycaemia induced a striking AVP increase in the normal controls.(ABSTRACT TRUNCATED AT 400 WORDS)

Adult↗

PubMed1994

Naloxone enhances angiotensin II-induced increase in serum luteinizing hormone concentrations in normal women.

The present study was carried out in order to establish whether the stimulatory effect of angiotensin II (ANG II) on serum concentration of LH in women is under control by endogenous opioid peptides. For this purpose, the effect of ANG II (infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg/min; each dose for 20 min) on serum LH levels was evaluated during administration of saline or the opioid antagonist naloxone (4 mg in an i.v. bolus followed by 10 mg over 2 h) in 7 normal women in both follicular and luteal phase. In all subjects, tests with saline alone (control test) or naloxone alone were performed. No significant changes in LH levels were observed in any test performed in the follicular phase and in the control test performed in the luteal phase. In contrast, in the luteal phase, both ANG II and naloxone induced significant increments in LH levels (23% increase vs. baseline by ANG II and 54% by naloxone). When naloxone and ANG II were given together stimulated LH increase was greatly enhanced. The mean peak was 154% higher than baseline and was higher than the sum of the individual peaks produced by naloxone and ANG II alone. These findings suggest inhibition by endogenous opioids of the stimulating action of ANG II on LH secretion during the luteal phase.

Adult↗

PubMed1994

Oxytocin response to challenging stimuli in elderly men.

The present study was carried out in order to establish possible alterations in oxytocin (OT) secretion with aging. Therefore, we evaluated the OT responses to insulin (0.15 U/kg)-induced hypoglycemia or to the administration of angiotensin II (i.v. infusion for 60 min of successively increasing doses of 4, 8 and 16 ng/kg min; each dose for 20 min) or apomorphine (60 micrograms/kg s.c.) in male subjects aged 22-80 yr and divided into 3 groups by age (group I (n = 9): 22-38 yr; group II (n = 9): 41-60 yr; group III (n = 9): 63-80 yr). Basal OT concentrations were similar in all groups. The OT response during the insulin tolerance test and the administration of ANG II had similar patterns and magnitudes in all groups. The OT response to apomorphine was similar in the two younger groups, with plasma OT levels increased 118% vs. baseline. In contrast, apomorphine was unable to induce a significant OT rise in the oldest group. During apomorphine test plasma OT concentrations were significantly lower in group III than in groups I and II. For the first time in elderly human subjects, these data show normal responsiveness of the OT secretory system to releasing stimuli such as hypoglycemia and ANG II. These findings indicate that in aged men production of OT and capability of responding to challenging stimuli is unchanged. On the other hand, the reduced OT responsiveness to apomorphine in group III might be an expression of the general dopaminergic dysfunction affecting the aging brain.

Adult↗