The aim of our study was to elucidate the physiological role of the neuropeptide galanin in the regulation of anterior pituitary function in human subjects. Six healthy men (age range 26-35 yr, body mass index range 20-24 kg/m2) underwent in random order 1) an intravenous bolus injection of growth hormone-releasing hormone (GHRH)-(1-29)-NH2 (100 micrograms) + thyrotropin-releasing hormone (TRH, 200 micrograms) + luteinizing hormone-releasing hormone (LHRH, 100 micrograms) + corticotropin-releasing hormone (CRH, 100 micrograms), and 2) intravenous saline (100 ml) at time 0 plus either human galanin (500 micrograms) in saline (100 ml) or saline (100 ml) from -15 to +30 min. Human galanin determined a significant increase in serum GH (GH peak: 11.3 +/- 2.2 micrograms/l) from both baseline and placebo levels. No significant differences were observed between GH values after galanin and those after GHRH alone (24.3 +/- 5.2 micrograms/l). Human galanin significantly enhanced the GH response to GHRH (peak 49.5 +/- 10 micrograms/l) with respect to either GHRH or galanin alone. Human galanin caused a slight decrease in baseline serum adrenocorticotropic hormone (ACTH; 16.3 +/- 2.4 pg/ml) and cortisol levels (8 +/- 1.5 micrograms/dl). Galanin also determined a slight reduction in both the ACTH (peak 27 +/- 8 pg/ml) and cortisol (peak 13.8 +/- 1.3 micrograms/dl) responses to CRH. Baseline and releasing hormone-stimulated secretions of prolactin, thyroid-stimulating hormone, LH, and follicle-stimulating hormone were not altered by galanin. Our data suggest a physiological role for the neuropeptide galanin in the regulation of GH secretion in humans.(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of our study was to investigate the effect of hexarelin, a novel GH-releasing peptide-6 analog, and GH-releasing hormone (GHRH) (alone or in combination) on GH secretion in adult patients with increased somatostatin tone due to chronic glucocorticoid excess. We studied seven adult patients undergoing long-term (no less than 6 months) immunosuppressive glucocorticoid treatment for non-endocrine diseases (six females and one male, age range 42-68 years) and one subject (female, age 31 years) with endogenous hypercortisolism due to adrenal adenoma. Six normal subjects (four females and two males) matched for sex and age with the patients and not undergoing any therapy served as controls. All the subjects underwent the following three tests in random order: (1) human GHRH (1-29)NH2 (100 micrograms in 1 ml saline) injected as an i.v. bolus at 0 min, (2) hexarelin (100 micrograms in 1 ml saline) injected as an i.v. bolus at 0 min and (3) hexarelin (100 micrograms in 1 ml of saline) plus GHRH (100 micrograms in 1 ml saline) injected as an i.v. bolus at 0 min. After GHRH alone the patients with glucocorticoid excess showed a blunted GH response as compared with normal subjects (median delta GH: 0.9, range 0-5.6 micrograms/l vs 7:1, range 0.3-14.9 micrograms/l). No significant differences were observed in the steroid-treated group with respect to normal subjects after hexarelin alone (median delta GH: 15.5, range 1.9-45.2 micrograms/l vs 17.9, range 5.5-53.9 micrograms/l).(ABSTRACT TRUNCATED AT 250 WORDS)

The aim of our study was to evaluate the effect of the iv administration of two different beta 2- receptors agonists, salbutamol and broxaterol, on the growth hormone (GH) response to maximal exercise in 11 patients (8 males and 3 females; age range 18-65 yr; mean +/- SE age 56 +/- 13 yr; BMI 26.2 +/- 1.4 kg/m2) with chronic asthmatic bronchitis. All the subjects underwent four cycloergometric exercise tests (incremental workload until maximal predicted heart rate). At baseline, at maximal exercise, at the end of the recovery period and 60 min after the end of each exercise, blood samples were drawn for the assay of GH, glucose, insulin, lactates, norepinephrine and epinephrine. Two exercises were performed without treatment while the remaining two were performed 60 min after the administration of 400 micrograms of either salbutamol or broxaterol (both diluted in 10 ml of saline) according to a randomized double blind cross-over design. Both exercise tests performed without treatment caused a significant (p < 0.05) and similar GH peak with respect to baseline values (from 0.3 +/- 0.1 micrograms/L to 2.8 +/- 1.3 micrograms/L, mean of the two exercise tests). Salbutamol pretreatment blunted the GH response to exercise which caused a no more significant serum GH peak over the baseline levels (from 0.6 +/- 0.2 micrograms/L to 1.4 +/- 0.6 micrograms/L,). Moreover, broxaterol completely abolished the GH response to exercise (baseline level 0.6 +/- 0.2 micrograms/L; peak levels 0.4 +/- 0.1 micrograms/L). The serum GH peak after exercise + broxaterol was significantly (p < 0.05) lower as compared to exercise + salbutamol. In conclusion, we have demonstrated for the first time that beta 2 stimulation blunts the physiological GH response to maximal exercise in adult human subjects. It can be suggested that changes in brain neurotransmitters, possibly an increase in the alpha-adrenergic tone, are likely to be involved in this endocrine effects of exercise.

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