The interactive effects of androgen exposure during neonatal and adult life on the pattern of GH secretion in adult male rats was investigated. Neonatal rats were orchidectomized or sham-operated on days 1-2 of life and injected immediately postoperatively with testosterone propionate (250 micrograms, sc) or vehicle. At 90-130 days of age the rats were bled every 20 min between 9 and 17 h from an indwelling intraatrial catheter. Some neonatally gonadectomized, testosterone- or vehicle-treated rats were also given depot testosterone (15 mg/kg, im) 5-10 days before blood sampling. Plasma GH concentrations were measured by RIA, and the pulsatile secretory patterns were analyzed by the PULSAR computer program. Neonatal orchidectomy resulted in a marked suppression (50-75%) of both the height and duration of GH secretory episodes, while baseline GH levels were higher in neonatally gonadectomized males than in sham-operated controls. Neonatal testosterone replacement therapy restored high amplitude GH pulses. However, the GH pulses of these animals were of significantly shorter duration and occurred more frequently, and baseline GH levels were markedly higher than those in intact male rats. In contrast, neonatally gonadectomized rats treated with testosterone both neonatally and during adulthood exhibited a GH pattern indistinguishable from that in normal males, with high amplitude and long-lasting (103 +/- 8 min) pulses at regular intervals (178 +/- 9 min). A similar masculine GH pattern was seen in neonatally gonadectomized rats given testosterone only during adult life. The present results indicate that high amplitude GH pulses can be induced by either neonatal or adult androgen exposure. However, while neonatal androgens irreversibly cause stimulation of overall GH secretion, only the continuous presence of androgens during adult life can induce a GH secretory pattern, consisting of large surges at regular 3-h intervals separated by a low baseline that is characteristic of normal male rats.