J. Raza et al., DIRECT EFFECTS OF CORTICOTROPIN-RELEASING HORMONE ON STIMULATED GROWTH-HORMONE SECRETION, Clinical endocrinology, 48(2), 1998, pp. 217-222
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.