DIRECT EFFECTS OF CORTICOTROPIN-RELEASING HORMONE ON STIMULATED GROWTH-HORMONE SECRETION

Citation
J. Raza et al., DIRECT EFFECTS OF CORTICOTROPIN-RELEASING HORMONE ON STIMULATED GROWTH-HORMONE SECRETION, Clinical endocrinology, 48(2), 1998, pp. 217-222
Citations number
29
Categorie Soggetti
Endocrynology & Metabolism
Journal title
ISSN journal
03000664
Volume
48
Issue
2
Year of publication
1998
Pages
217 - 222
Database
ISI
SICI code
0300-0664(1998)48:2<217:DEOCHO>2.0.ZU;2-P
Abstract
OBJECTIVE This study evaluated the effect of corticotrophin-releasing hormone (CRH) on growth hormone releasing hormone (GHRH)-stimulated gr owth hormone (GH) release in man. DESIGN Six healthy adult volunteers (age 20-35 years) were studied. On different occasions they each recei ved an intravenous bolus of saline, CRH(1-41) (100 mu g), adrenocortic otrophic hormone (ACTH) [Synacthen (500ng/m(2))] or hydrocortisone (50 mg), followed 30 minutes rater by an intravenous bolus of either GHRH- (1-29)-NH2 (1.0 mu g/kg) or saline. MEASUREMENT Serum GH concentration s were measured using an immunoradiometric assay, and cortisol concent rations were measured by commercial radioimmunoassay. TSH concentratio ns were measured using a solid phase immunoradiometric assay kit. RESU LTS Pretreatment with CRH(1-41) attenuated the GH response to GHRH [sa line/GHRH-(1-29)-NH2 20.2 +/- 6.2 mU/l; CRH(1-41)/GHRH-(1-29)-NH2 10.9 +/- 2.8 mU/l (P = 0.01)]. This effect was not due to the rise in ACTH or cortisol induced by CRH(1-41), since pretreatment with either ACTH or hydrocortisone significantly augmented the GH response to GHRH-(1- 29)-NH2 in the same subjects [ACTH/GHRH-(1-29)-NH2 30.3 +/- 8.8 mU/l ( P = 0.01); hydrocortisone/GHRH-(1-29)-NH2 36.4 +/- 11.2 mU/l (p = 0.02 )]. CONCLUSION Our data suggest that the inhibitory effect of CRH(1-41 ) on GHRH-(1-29)-NH2-induced GH release is not a result of ACTH or cor tisol release but reflects a direct action of CRH on GH secretion, pos sibly via stimulation of somatostatin release. The acute rise in GH fo llowing glucocorticoid administration could be explained in part by a rapid suppression of endogenous CRH.