Recent evidence has shown that growth hormone-releasing hormone (GHRH) enables investigation of the pathophysiology of GH secretion in a variety of different states, but it cannot be used as a test for probing pituitary somatotrophic function, due to the extreme inter- and intra-subject variability in normal subjects. This task is better accomplished when compounds which deprive the pituitary of inhibitory (somatostatinergic) influences, e.g. pyridostigmine, arginine, etc., are given in combination with GHRH. Administration of GHRH in both animals and humans reveals a state of GH hyperresponsiveness in the immediate postnatal period, which is likely to be due to a reduced pituitary sensitivity to somatostatin. GH responses to GHRH are relatively constant throughout the different stages of pubertal development, though further studies are needed to confirm these findings, and decline after the third-fourth decade in men, after menopause in women. It is apparent that during aging the releasable pool of GH is preserved and that impaired GH secretion is due to defective hypothalamic GHRH function and a relative predominance of somatostatinergic function.