OBJECTIVE: Chronic hypercortisolism is associated with decreased GH responsiveness to GHRH. GHRP-6 is a synthetic hexapeptide that releases GH in several species, including man. As GHRH and GHRP-6 apparently stimulate GH release by different mechanisms, we evaluated the GH responses to these peptides in patients with endogenous and exogenous glucocorticoid excess and also in control subjects. DESIGN: Six patients with endogenous hypercortisolism, nine with exogenous glucocorticoid excess and 10 normal controls were submitted to three tests, in random order, with GHRH (100 micrograms), GHRP-6 (1 microgram/ kg) or GHRP+GHRP-6, in the same doses, i.v., on separate days. MEASUREMENTS: GH was measured by immunofluorometric assay. IGF-I was determined by radioimmunoassay. Plasma glucose was measured by the glucose-oxidase technique. RESULTS: Peak GH values (mean +/- SE; microgram/l) after GHRH were significantly blunted in endogenous (2.0 +/- 0.7) and exogenous (3.6 +/- 1.2) hypercortisolaemic patients compared to controls (24.9 +/- 6.1). The endogenous group had lower peak GH values after GHRP-6 alone (7.7 +/- 1.9) or together with GHRH (18.8 +/- 5.8) than those observed in controls (GHRP-6: 22.1 +/- 3.6; GHRH+GHRP-6: 77.4 +/- 15.0) and in exogenous hypercortisolism (27.4 +/- 6.2 and 78.1 +/- 19.9). There were no differences in the GH responses to GHRP-6 alone or in combination with GHRH when controls were compared to the exogenous group. No changes in plasma IGF-I and glucose levels were observed. CONCLUSIONS: Our results suggest that hypercortisolism had a different effect on the GH-releasing mechanisms stimulated by GHRH and GHRP-6. Moreover, in endogenous hypercortisolism both GHRH and GHRP-6 pathways are affected, while in the exogenous group GHRP-6 releasing mechanisms are apparently preserved.
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Borges et al. (1997) studied this question.