Patients with hyperthyroidism have reduced growth hormone (GH) responses to pharmacological stimuli and reduced spontaneous nocturnal GH secretion. The stimulatory effect of clonidine on GH secretion has been suggested to depend on an enhancement of hypothalamic GH-releasing hormone (GHRH) release. The aim of our study was to evaluate the effects of clonidine and GHRH on GH secretion in patients with hyperthyroidism. Eight hyperthyroid females with recent diagnosis of Graves’ disease (age range 20–55 years, body mass index range 19.2–26.2 kg/m<sup>2</sup>) and 6 healthy female volunteers (age range 22–35 years, body mass index range 19–25 kg/m<sup>2</sup>) underwent two experimental trials at no less than 7-day intervals: (a) an intravenous infusion of clonidine 150 µg in 10 ml of saline, or (b) a bolus intravenous injection of human GHRH (1–29)NH<sub>2</sub>, 100 µg in 1 ml of saline. Hyperthyroid patients showed blunted GH peaks after clonidine (7.1 ± 1.7 µg/l) as compared to normal subjects receiving clonidine (28.5 ± 4.9 µg/l, p < 0.05). GH peaks after GHRH were also significantly lower in hyperthyroid subjects (8.0 ± 1.7 µg/l) as compared to normal subjects receiving GHRH (27.5 ± 4.4 µg/l, p < 0.05). No significant differences in the GH values either after clonidine or GHRH were observed in the two groups of subjects examined. Our data demonstrate that the GH responses to clonidine as well as to GHRH in patients with hyperthyroidism are inhibited in a similar fashion with respect to normal subjects. That clonidine is not able to reverse the blunted GH secretion in hyperthyroidism suggests that hyperthyroxinemia may either cause an increase in somatostatin release by the hypothalamus or block GH secretion acting directly at the pituitary level.