EFFECT OF TESTOSTERONE REPLACEMENT THERAPY ON THE SOMATOTROPE RESPONSIVENESS TO GHRH ALONE OR COMBINED WITH PYRIDOSTIGMINE AND ON SYMPATHOADRENAL ACTIVITY IN PATIENTS WITH HYPOGONADISM

There is evidence suggesting that androgens influence GH secretion in man. Our aim was to verify whether the GH releasable pool is preserved and influenced by testosterone replacement in male hypogonadism. To t his goal, in eight male hypogonadal patients (HP, age 32.2+/-5.0 yr; B ody Mass Index 23.9+/-1.1 kg/m(2)) before and after 3 months testoster one therapy, we studied the GH response to GHRH (1 mu/kg iv) alone and combined with pyridostigmine (PD, 120 mg po), a cholinesterase inhibi tor which likely inhibits hypothalamic somatostatin release allowing e xploration of the maximal somatotrope secretory pool. Sixteen normal s ubjects (NS, age 30.1+/-3.5 yr; Body Mass Index 22.5+/-1.8 kg/m(2)) we re studied as controls. The GH response to GHRH in HP was similar to t hat in NS (AUG, mean+/-SE: 1238+/-362 vs 1018+/-182 mu g/L/h). PD pote ntiated to the same extent the GH response to GHRH in both groups (209 2+/-807 and 2840+/-356 mu g/L/h). After three month testosterone thera py, in HP the GH responses to GHRH alone (1352+/-612 mu g/L/h) and com bined with PD (1948+/-616 mu g/L/h) were unchanged. Also IGF-I levels in HP were similar to those in NS (222+/-42 vs 210.6+/-55.8 mu g/L) an d were unchanged during testosterone replacement (280+/-31 mu g/L). As androgens have been reported to modulate sympathoadrenal activity in the rat, both before and during testosterone replacement, we also meas ured plasma catecholamine levels, Basal NE (p< 0.05) but not E levels were lower in HP than in NS; testosterone restored basal NE levels to normal without affecting basal E. Delta absolute increase of NE and E (p<0.05 and 0.01 vs baseline, respectively) after PD in HP were simila r to those in NS and were unchanged during testosterone replacement. I n conclusion, these results demonstrate that the GH releasable pool is preserved in male hypogonadism, As in this condition a reduction of s pontaneous GH secretion has been reported, it could be due to neurosec retory dysfunction but not to pituitary impairment, Subtle alterations of sympathoadrenal activity seem to be present in male hypogonadism a nd reversed by testosterone replacement.