Effects of glucocorticoid treatment and acute passive immunization with growth hormone-releasing hormone and somatostatin antibodies on endogenous and stimulated growth hormone secretion in the male rat J.
Miell, R. Corder, P. J. Miell, C. McClean and R. C. Gaillard
Neuroendocrine Unit, Department of Medicine, University Hospital of Geneva, 1211 Geneva 4, Switzerland *Protein Hormone Unit, St Bartholomew's Hospital, London ecia 7be (Requests for offprints should be addressed to J. Mieli now at Department of Medicine, King's College School of Medicine, Bessemer Road, London se5 9pj) received
6
February
1991
ABSTRACT
Despite causing marked inhibition of somatic growth, glucocorticoids enhance both the response to GH\x=req-\ releasing hormone (GHRH) and the amplitude of naturally occurring GH secretory pulses in the male rat. The relative contribution of the two major hypothalamic regulatory factors for GH (somatostatin and GHRH) to these observed effects remains speculative. In the present studies, we have investigated endogenous and stimulated GH release in rats pretreated with glucocorticoid or vehicle, and the effects of passive immunoneutralization of
somatostatin or GHRH. In an initial study, four groups of eight rats were treated with either saline or various doses of a depot preparation of betamethasone: low dose, 0\m=.\85mg; medium dose, 1\m=.\7mg; high dose, 3\m=.\4mg. All doses
significantly suppressed body weight gain, total adrenal weight and concentrations of both plasma corticosterone and pituitary ACTH. Seven days after
betamethasone treatment, GH responses to an i.v. injection of 1 \g=m\ghuman GHRH(1\p=n-\29)were evaluated during pentobarbitone anaesthesia. Compared with saline-treated controls (peak GH concentration of 506\m=.\0\m=+-\68\m=.\5\g=m\g/l),peak GH levels were enhanced by the low dose (704\m=.\4\m=+-\47\m=.\8\g=m\g/l,P
Miell, R. Corder, P. J. Miell, C. McClean and R. C. Gaillard
Neuroendocrine Unit, Department of Medicine, University Hospital of Geneva, 1211 Geneva 4, Switzerland *Protein Hormone Unit, St Bartholomew's Hospital, London ecia 7be (Requests for offprints should be addressed to J. Mieli now at Department of Medicine, King's College School of Medicine, Bessemer Road, London se5 9pj) received
6
February
1991
ABSTRACT
Despite causing marked inhibition of somatic growth, glucocorticoids enhance both the response to GH\x=req-\ releasing hormone (GHRH) and the amplitude of naturally occurring GH secretory pulses in the male rat. The relative contribution of the two major hypothalamic regulatory factors for GH (somatostatin and GHRH) to these observed effects remains speculative. In the present studies, we have investigated endogenous and stimulated GH release in rats pretreated with glucocorticoid or vehicle, and the effects of passive immunoneutralization of
somatostatin or GHRH. In an initial study, four groups of eight rats were treated with either saline or various doses of a depot preparation of betamethasone: low dose, 0\m=.\85mg; medium dose, 1\m=.\7mg; high dose, 3\m=.\4mg. All doses
significantly suppressed body weight gain, total adrenal weight and concentrations of both plasma corticosterone and pituitary ACTH. Seven days after
betamethasone treatment, GH responses to an i.v. injection of 1 \g=m\ghuman GHRH(1\p=n-\29)were evaluated during pentobarbitone anaesthesia. Compared with saline-treated controls (peak GH concentration of 506\m=.\0\m=+-\68\m=.\5\g=m\g/l),peak GH levels were enhanced by the low dose (704\m=.\4\m=+-\47\m=.\8\g=m\g/l,P
