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Biomedical subjects

A Giustina

Publications and source records attributed to A Giustina.

At least 109 records · Page 6Linked to original sources
PubMed1994

Effects of beta 2-agonists during cardiopulmonary exercise test in COPD patients.

The aim of this study was to evaluate endocrine-metabolic, respiratory and cardiovascular effects of two beta 2-sympathomimetic selective agents, such as broxaterol and salbutamol, before and during cardiopulmonary exercise test (CPX). Twelve in-patients with chronic obstructive pulmonary disease (COPD) (with partially reversible airways obstruction) were included. Broxaterol (400 micrograms) and salbutamol (400 micrograms) were administered i.v., according to a double-blind, cross-over study. Before treatment and within 60 min after the administration of each agent, the patients underwent incremental CPX by bicycle ergometer to the maximum tolerable threshold. At these times the following variables were assessed: minute ventilation (VE), oxygen consumption (VO2), carbon dioxide production (VCO2), VE/VO2 ratio and O2 pulse, glycaemia, insulinaemia, plasma norepinephrine (NE) and epinephrine (E), arterial oxygen and carbon dioxide tension (PaO2 and PaCO2), plasma lactates, heart rate (HR), systolic (SBP) and diastolic (DBP) blood pressure. Spirometry was performed before and after the administration of each beta 2-adrenoceptor agonist. CPX brought about a significant increase in VE, VO2, VCO2, and O2 pulse. Broxaterol or salbutamol administration did not significantly modify the increases caused by CPX. At rest, 60 min after treatment, both bronchodilators caused a significant rise in glycaemia. A significant reduction of PaO2 (after broxaterol) and PaCO2 (after salbutamol) was observed at rest. In contrast, both agents caused no modification to potassium and insulin levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1993

Variability in the growth hormone response to growth hormone-releasing hormone alone or combined with pyridostigmine in type 1 diabetic patients.

In man the GH response to GHRH is variable within and between subjects. Pyridostigmine (PD), an acetylcholinesterase inhibitor, has been shown to reduce the variability of the GH response to GHRH in normal subjects. The aim of this study was to assess the existence of either inter- or intraindividual variability in the GH response to GHRH in type 1 diabetic patients. Moreover, we investigated the effect of PD on such variability in the same patients. Seven (4 females-3 males) nonobese type 1 diabetic patients underwent two experiments performed in consecutive days according to a single-blind protocol: 1) 120 mg oral PD 60 min before iv injection of human (h) GHRH-(1-29) NH2, 100 micrograms in 2 ml of sterile water; 2) oral placebo 60 min before iv injection of 100 micrograms hGHRH. The two experiments were then repeated, following the same procedure, one and two weeks after the start of the study. The GH peaks after GHRH were variable within different subjects but also in the same subject on different occasions. However, the mean GH peak levels after GHRH in the three tests were not significantly different (14.2 +/- 3.5, 15.3 +/- 3, 16.5 +/- 6.4 micrograms/L, respectively), the coefficient of variation for each test was 65%, 51.8%, 102.4%, respectively (mean 73.1 +/- 15.1%). The GH response to GHRH was always significantly enhanced by PD administration: the mean GH peak levels in the three tests were 31.9 +/- 7.1, 44.8 +/- 10.4, 49.9 +/- 13.1 micrograms/L, respectively, without significant differences between tests.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Hypothalamic regulation of growth hormone secretion during food deprivation in the rat.

Suppressed pulsatile GH secretion in food-deprived rats has been hypothesized to be due to an increase in hypothalamic somatostatin secretion. We investigated this hypothesis and the role of GHRH in regulating GH secretion during food deprivation using two different models. In experiment one, rats were food deprived for 72h during which time they received a saline infusion (n = 5). At the same time rats were normal fed for 72h during which time they received a somatostatin infusion (5 micrograms/h, n = 7). After the 72h infusion period, all rats received two iv injections of GHRH (1 microgram/rat) at 2h intervals. GH concentrations in food-deprived rats rose from approximately 10 ng/ml to 400-800 ng/ml in response to both GHRH injections. This increase was significantly greater (p < 0.01) than the GH response (100-400 ng/ml) observed in somatostatin-infused animals. The significantly higher GH response observed in food-deprived rats as compared to somatostatin-infused, normal-fed rats suggests that somatostatin concentrations may decrease during food deprivation. In experiment two, rats were infused for 5h with either saline (n = 6) or GHRH (10 micrograms/h, n = 9) at the end of a 72h fast. GH concentrations did not change in saline-infused animals. In contrast, GH concentrations significantly increased (p < 0.01) upon initiation of the continuous GHRH infusion. Yet, this release of GH was pulsatile in nature. Pulsatile GH secretion in the presence of a constant GHRH infusion suggests that pulsatile somatostatin release from the hypothalamus is maintained during food deprivation. These studies suggest that during food deprivation in the rat 1) absolute concentrations of somatostatin decrease, but its pattern of secretion remains pulsatile, and 2) decreased GHRH release may be responsible for the absence of spontaneous GH pulses.

Animals↗
PubMed1993

Arginine blocks the inhibitory effect of hydrocortisone on circulating growth hormone levels in patients with acromegaly.

In patients with acromegaly, circulating growth hormone (GH) levels and GH responses to GH-releasing hormone (GHRH) are decreased by long-term administration of pharmacological doses of glucocorticoids. The aim of our study was to investigate the acute effects of intravenous (i.v.) infusion of hydrocortisone combined either with saline or arginine infusion on circulating GH levels in acromegaly. We studied five adult patients with acromegaly, two men and three women aged 54.6 +/- 4 years having a body mass index of 25.9 +/- 1.2 kg/m2. On two randomized occasions, patients underwent a bolus i.v. injection of 100 mg hydrocortisone succinate at time 0 followed by a 120-minute i.v. infusion of 250 mg hydrocortisone in 250 mL saline, combined with a 90-minute (from -15 to 75 minutes) i.v. infusion of (1) 60 g arginine hydrochloride in 200 mL saline, or (2) 200 mL saline. In all of the acromegalic patients during the infusion of hydrocortisone alone, serum GH levels clearly decreased (nadir range, 26.4% to 68.1%) with respect to GH levels before hydrocortisone administration (mean of time -15 and 0, basal level), with a nadir between 90 and 180 minutes after the beginning of the infusion. After arginine pretreatment, GH levels were significantly enhanced compared with levels attained with hydrocortisone saline, and they were also significantly increased (peak, 167.5% +/- 27.7%) with respect to basal levels. Our data show that arginine blocks the inhibitory effect of acute and sustained hypercortisolism on circulating GH levels in acromegaly.(ABSTRACT TRUNCATED AT 250 WORDS)

Acromegaly↗
PubMed1993

Effects of metoclopramide on the growth hormone response to galanin in normal man.

One of the most prominent metabolic effects of the systemic administration of the synthetic neuropeptide galanin in man is the increase in growth hormone (GH) secretion. This stimulating action of galanin is thought to occur directly at the hypothalamic level through the release of GHRH. Recently, it has been shown that also dopaminergic drugs may elicit GH secretion through an increase in hypothalamic GHRH secretion. The aim of this study was to investigate if the action of galanin on GHRH and consequently on GH release may be mediated via dopaminergic pathways evaluating the effects of a potent central dopaminergic receptor blocker, metoclopramide (MCP), on the galanin-induced growth hormone (GH) secretion in normal subjects. We studied seven young non obese healthy subjects (three females and four males). GH secretion was evaluated after 45 min iv infusion of porcine galanin (0.5 mg in 100 ml of saline) from 0 to 45 min combined with a 60 min iv infusion of a) saline (100 ml) or b) MCP (10 mg in 100 ml of saline) from -15 to 45 min. In all the seven subjects, during galanin infusion, GH values increased with respect to baseline with peaks occurring between 30 and 60 min after the beginning of galanin infusion. Peak GH values ranged between 3.5 and 15.4 micrograms/l (mean 10.4 +/- 1.6 micrograms/l). During MCP infusion no significant differences in the GH response to galanin with respect to saline were observed both when absolute GH levels and GH AUC were examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of metoclopramide on the paradoxical growth hormone response to galanin in acromegaly.

Galanin is able to enhance growth hormone (GH)-releasing hormone stimulated GH secretion in normal man. In acromegaly circulating GH levels are elevated and the GH response to GHRH may be exaggerated. Galanin has been recently shown to decrease circulating GH levels in acromegaly. Dopaminergic drugs were the only previously known agents able to cause a paradoxical GH fall in acromegaly. Aim of our study was to investigate the effects of a potent central dopaminergic receptor blocker, metoclopramide (MCP), on the galanin-induced paradoxical GH secretion in acromegalic subjects. Two male and three female patients with active acromegaly (age range 44-66 years, body mass index range 24.6-28 Kg/m2) were studied after 45 min i.v. infusion of porcine galanin (0.5 mg in 100 ml of saline) from 0 to 45 min combined with a 60 min i.v. infusion of a) saline (100 ml) or b) MCP (10 mg in 100 ml of saline) from -15 to 45 min. After galanin, GH values fell from baseline (27.5 +/- 10 micrograms/L) to a mean nadir of 16.4 +/- 6.1 micrograms/L; after galanin + MCP, circulating GH levels were also decreased (mean nadir 17.3 +/- 8.1 micrograms/L) in all the patients with respect to baseline (23.6 +/- 9.7 micrograms/L). No significant differences were found in absolute or percent of baseline GH levels after galanin+saline vs galanin + MCP. Our results suggest that the paradoxical GH fall after galanin in acromegalic patients is not mediated through dopaminergic receptor. It can be hypothesized that galanin may interact at the pituitary level with its own receptors expressed by GH-secreting adenomatous cells.

Acromegaly↗
PubMed1993

Effect of galanin on the growth hormone (GH) response to GH-releasing hormone in patients with Cushing's disease.

Attenuated plasma GH secretion during sleep and blunted GH responses to provocative stimuli have been observed in patients with Cushing's disease. Synthetic porcine galanin elicits GH secretion when given alone, and enhances the GH response to GHRH in normal human subjects. The aim of our study was to investigate the effects of galanin on the GH response to GHRH in patients with Cushing's disease. We studied 5 female subjects with untreated active Cushing's disease caused by micro-pituitary adenomas (age 43 +/- 6.7 years; BMI 30 +/- 0.7 kg/m2). Four normal adult females, matched for age and body weight with the patients with Cushing's disease, were studied as controls. Subjects underwent in random order: (1) infusion of synthetic porcine galanin IV, 500 micrograms in 100 mL; (2) infusion of saline, IV, 100 mL. A bolus of human GHRH(1-29)NH2 (Geref, Serono, Italy), 100 micrograms in 1 mL saline, was injected IV at 0 minutes. Patients with Cushing's disease showed blunted GH peaks after GHRH (1.2 +/- 0.4 micrograms/L) during saline infusion, as compared to normal controls (24.6 +/- 4.6 micrograms/L; p < 0.05). During galanin infusion a significantly enhanced GH response to GHRH, as compared with saline infusion, was observed in control subjects (GH peak: 51.4 +/- 9.8 micrograms/L; p < 0.05), but not in patients with Cushing's disease (GH peak: 2.3 +/- 0.6 micrograms/L). GH levels were significantly lower both after saline and after galanin in patients with Cushing's disease as compared to normal controls. Our data demonstrate that galanin is not able to enhance the GH response to GHRH in patients with Cushing's disease. That galanin cannot reverse this effect suggests that the mechanism of action of galanin is not via a decrease in somatostatin release by the hypothalamus.

Adenoma↗
PubMed1993

Effect of galanin and arginine, alone or in combination, on growth hormone secretion in adult patients treated with glucocorticoids.

Glucocorticoids are known to decrease growth hormone (GH) secretion in man. Galanin, a 29-amino acid peptide, and arginine stimulate GH secretion through different hypothalamic mechanisms. The aim of our study was to investigate the effect of arginine and galanin (alone or in combination) on GH secretion in 7 adult patients with nonendocrine diseases receiving chronic daily immunosuppressive glucocorticoid treatment (5 F, 2 M; mean age 48.4 +/- (SEM) 3.7 years). Five normal adults (3 F, 2 M; mean age 34.6 +/- 2.2 years) served as controls. All subjects underwent in random order: (1) infusion of arginine hydrochloride (30 g i.v. in 100 ml saline) from -30 to 0 min; (2) infusion of synthetic porcine galanin (500 micrograms i.v. in 100 ml saline) from -15 to 30 min; (3) intravenous infusion of arginine hydrochloride from -30 to 0 min combined with synthetic porcine galanin from -15 to 30 min. In normal subjects GH peak after arginine (8.6 +/- 3.3 micrograms/l) and galanin (6.6 +/- 3.2 micrograms/l) did not show significant differences; the GH peak after arginine + galanin (21.4 +/- 6.1 micrograms/l) was significantly higher with respect to galanin or arginine alone. In glucocorticoid-treated patients the GH peak after arginine (4.6 +/- 1.5 micrograms/l) was significantly (p < 0.05) higher with respect to galanin (1.8 +/- 1.0 micrograms/l); after arginine + galanin the GH peak (8.2 +/- 2.3 micrograms/l) was significantly (p < 0.05) enhanced with respect to either galanin or arginine alone. The GH response to arginine was not significantly different in normal and glucocorticoid-treated patients.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effects of sex and age on the growth hormone response to galanin in healthy human subjects.

The aim of our study was to analyze the effects of sex and age on the GH response to galanin infusion in healthy subjects. We have studied 12 young (age, < 40 yr) nonobese healthy volunteers [6 females: age, 31.0 +/- 2.5 yr; body mass index (BMI), 21.6 +/- 0.9 kg/m2; 6 males: age, 29.2 +/- 1.4 yr; BMI, 23.3 +/- 0.4 kg/m2] and 11 old (age, > 65 yr) healthy subjects (5 females: age, 83.8 +/- 3.8 yr; BMI, 23.4 +/- 1.4 kg/m2; 6 males: age, 79.7 +/- 4.6 yr; BMI, 23.3 +/- 0.2 kg/m2). All subjects received an infusion of synthetic porcine galanin (500 micrograms, iv) in 100 mL saline from 0-45 min. Blood samples for GH measurement were drawn at -15, 0, 15, 30, 45, 60, 90, and 120 min. The GH peaks after galanin treatment in young females (11.9 +/- 2.9 micrograms/L) were significantly (P < 0.05) higher than those in the young males (5.1 +/- 1.8 micrograms/L). Old males showed significantly higher peak GH levels after galanin treatment (8.6 +/- 3.1 micrograms/L) than old females (2.4 +/- 0.6 micrograms/L). The GH peaks and areas under the curve after galanin treatment were significantly (P < 0.05) higher in young than in old females. On the contrary, no significant differences were observed after galanin treatment in young and old males. The magnitude of galanin-induced GH secretion significantly correlated with estradiol levels in young women. Our data seem to suggest that circulating estrogen levels play a crucial permissive role in galanin-induced GH secretion in humans.

Adult↗
PubMed1993

Effect of long-term treatment with bromocriptine on the growth hormone response to galanin in patients with acromegaly.

Galanin elicits growth hormone (GH) secretion in normal man but may cause a paradoxical fall of GH in acromegaly. The aim of our study was to investigate the effects of long-term treatment with bromocriptine on the galanin-induced GH decrease in acromegalic subjects. Six acromegalic patients (5F, 1M) chronically treated with bromocriptine underwent in randomized order: (i) iv infusion of 100 ml saline from 0 to 45 min and (ii) iv infusion of synthetic porcine galanin (0.5 mg in 100 ml saline) from 0 to 45 min. In acromegalic patients, GH values fell from baseline (10.5 +/- 2.7 micrograms/l) to a mean nadir of 6.9 +/- 2.2 micrograms/l after galanin infusion (57.8 +/- 9.4% vs basal levels). Saline infusion did not cause any change in circulating GH levels. The mean change in GH values with respect to baseline after galanin in these subjects significantly differed from that observed after saline from time 15 to 90 min. Serum prolactin levels were not significantly affected by galanin. Our results confirm that the dose of galanin capable of increasing plasma GH levels in normal subjects can decrease GH values in patients with acromegaly. Moreover, our data show that this paradoxical GH decrease induced by galanin can also be observed in patients chronically treated with bromocriptine. Therefore, the paradoxical decreasing effect of galanin on plasma GH levels in acromegaly seems not to be mediated via dopaminergic pathways.

Acromegaly↗
PubMed1993

Picotamide, a dual TXB synthetase inhibitor and TXB receptor antagonist, reduces exercise-induced albuminuria in microalbuminuric patients with NIDDM.

We investigated the short-term effect of the TXB inhibitor picotamide on albuminuria induced by exercise in 15 microalbuminuric (i.e., with UAE at rest between 20 and 200 micrograms/min) type II diabetic patients (12 men and 3 women, age 56 +/- 2, BMI 28 +/- 1 kg/m2) and in six normal age-matched control subjects. The diabetic subjects performed five submaximal exercise tests (90% of theoretical heart rate) on a cycle ergometer: the first two under basal conditions; the third and fifth after subjects had received picotamide (900 mg/day) or placebo (3 tablets/day) for 10 days; the fourth exercise always was performed after 10 days of wash-out. Control subjects performed two exercises: the first in baseline conditions and the second after 10 days of picotamide administration (900 mg/day). When diabetic patients were untreated, a significant (P < 0.05) increase in UAE with respect to baseline levels was observed immediately after and 1 h after the exercise test. After picotamide administration, UAE significantly decreased (P < 0.05) immediately after and 1 h after exercise, as compared with diabetic patients given a placebo. In normal subjects, exercise was followed by a slight increase in UAE, which was not significantly affected by picotamide administration. Our results show that short-term administration of picotamide is associated with a reduction in UAE after exercise in type II diabetes patients with microalbuminuria while at rest. Picotamide, a TXB synthetase and receptor inhibitor, may decrease exercise-induced albuminuria in diabetic patients through a reduction in circulating TXB levels and inhibition of TXB action, which in turn may act by lowering glomerular capillary hydraulic pressure.

Albuminuria↗
PubMed1993

Isradipine decreases exercise-induced albuminuria in patients with essential hypertension.

The aim of our study was to investigate the effects of exercise on albuminuria and blood pressure in patients with essential hypertension, and the short-term effect of the calcium channel blocker isradipine on exercise-induced albuminuria (UAE) and blood pressure in the same patients. Ten patients (7 males, 3 females) with essential hypertension were admitted to the study. The mean age was 54 +/- 2.7 years and the mean body mass index was 27 +/- 1 kg/m2. Patients performed two physical exercise tests on a cycloergometer. Workload was increased by 30 watts every 2 min until 90% of the theoretical maximal heart rate was achieved. This workload was maintained for 5 min. Samples for albuminuria assay were collected at the end of exercise and 1 h after exercise. The first physical exercise test was performed after 15 days of placebo washout; the second exercise was performed after 10 days of therapy with isradipine 5 mg once daily p.o. After 10 days of therapy with isradipine, UAE immediately after (31 +/- 8.3 micrograms/min) and 1 h after exercise (31.5 +/- 7.3 micrograms/min) were significantly (p < 0.05) lower as compared to the values found after placebo (37.1 +/- 9.3 micrograms/min; 43.5 +/- 9.9 micrograms/min). Our data show that short-term administration of the calcium channel blocker isradipine is able to cause a concomitant significant decrease in exercise-induced pressor and albuminuric response in patients with essential hypertension. The finding that short-term calcium channel blockade can reduce exercise-induced albuminuria in essential hypertensive patients suggests that progression of nephropathy in this early phase could be slowed by isradipine in these patients.

Albuminuria↗
PubMed1992

[A case of retroperitoneal leiomyosarcoma].

Leiomyosarcoma is a rare malignant tumour originating from the smooth muscular tissue in any part of the organism, including retroperitoneum where it is particularly aggressive. It is nearly always characterized by a silent development causing diagnostic delay. The results of the primary therapy, which is always surgical, are limited because of the tumoral mass extension and the high local aggressiveness. The Authors present a clinical case which was under their observation and seize the opportunity of making a revision of the literature about it.

Aged↗
PubMed1992

Effect of galanin on the growth hormone response to growth hormone-releasing hormone in acromegaly.

Galanin enhances growth hormone (GH)-releasing hormone (GHRH)-stimulated GH secretion in normal man. In acromegaly, circulating GH levels are increased and the GH response to GHRH may be exaggerated. Galanin has been recently shown to decrease circulating GH levels in acromegaly. The aim of our study was to investigate the effects of galanin on the GH response to GHRH in acromegalic subjects. Five acromegalic patients (three men and two women) and seven healthy adult subjects (five men and two women) were studied. GHRH-induced GH secretion was evaluated during a 40-minute intravenous (IV) infusion of saline (100 mL) or porcine galanin (12.5 micrograms/min in 100 mL saline). In normal subjects, delta GH levels after GHRH+porcine galanin administration (47 +/- 7.5 micrograms/L) were significantly higher in comparison to levels obtained with GHRH+saline (21.7 +/- 3.5 micrograms/L, P < .05). In acromegalic patients, GH responses to GHRH (delta GH, 18.8 +/- 8.6 micrograms/L) were not altered by galanin infusion (delta GH, 17.6 +/- 5 micrograms/L). Our results give the first evidence that the same dose of galanin that induces a significant enhancement of the GH response to GHRH in normal subjects has no effect on the GH response to GHRH in acromegalic patients. It can be hypothesized that galanin may interact at the pituitary level with its own receptors expressed by somatotropes independent of GHRH. Failure of galanin to enhance GH response to GHRH in acromegalic patients could be due to a change in function of the galanin receptor on GH-secreting adenomatous cells.

Acromegaly↗
PubMed1992

Effect of galanin on growth hormone-releasing hormone-stimulated growth hormone secretion in adult patients with nonendocrine diseases on long-term daily glucocorticoid treatment.

Glucocorticoids are thought to inhibit growth hormone (GH) secretion through an enhancement of endogenous somatostatin tone. The aim of our study was to evaluate the effect of galanin, a neuropeptide that stimulates GH secretion, on GH-releasing hormone (GHRH)-induced GH secretion in adult patients with nonendocrine diseases who were under daily immunosuppressive glucocorticoid therapy. Six normal subjects (four men, two women) and seven steroid-treated subjects (three men, four women) were studied. GHRH-induced GH secretion was evaluated during a 40-minute intravenous (i.v.) infusion of saline or porcine galanin (12.5 micrograms/min). During saline infusion, steroid-treated patients showed a blunted GH response to GHRH (GH peak, 8.1 +/- 2.8 micrograms/L), as compared with normal subjects (GH peak, 23.8 +/- 3.9 micrograms/L). During galanin infusion, the GH response to GHRH was significantly enhanced (GH peak, 46.6 +/- 9.4 micrograms/L, P less than .05), as compared with saline infusion in normal subjects. In contrast, galanin infusion did not enhance the GH response to GHRH (GH peak, 16.6 +/- 6.5 micrograms/L), as compared with saline infusion in steroid-treated patients. The area under the GH-response curves was also significantly (P less than .05) lower in steroid-treated subjects, as compared with normal subjects. Thus, galanin failed to normalize or enhance the GH response to GHRH in patients treated long-term with glucocorticoids. It can be hypothesized that galanin does not elicit GH secretion by decreasing hypothalamic somatostatin tone.

Adult↗
PubMed1992

Comparative effect of clonidine and growth hormone (GH)-releasing hormone on GH secretion in adult patients on chronic glucocorticoid therapy.

Glucocorticoids are thought to inhibit growth hormone (GH) secretion through an enhancement of endogenous somatostatin tone. The aim of our study was to evaluate the effects of GH-releasing hormone (GHRH) and clonidine, an alpha-2-adrenergic agonist which increases GH secretion acting at the hypothalamic level with an unknown mechanism, on GH secretion in seven adult patients (3M, 4F) with non endocrine diseases and on daily immunosuppressive glucocorticoid therapy. Eleven normal subjects (7M, 4F) served as controls. Steroid-treated patients showed a blunted GH response to GHRH (GH peak 8.3 +/- 3 micrograms/L) with respect to normal subjects (GH peak 19.3 +/- 2.4 micrograms/L). The GH responses to clonidine were also blunted (p less than 0.05) in steroid-treated patients (GH peak 5.8 +/- 2.8 micrograms/L) with respect to normal subjects (GH peak 17.6 +/- 2.3 micrograms/L). No significant differences between the GH responses to GHRH and clonidine were observed either in steroid-treated or in normal subjects. Clonidine is not able to enhance GH secretion similar to GHRH in patients chronically treated with steroids. It can be hypothesized that clonidine does not elicit GH secretion decreasing hypothalamic somatostatin tone.

Adult↗