In hyperandrogenic states an abnormal pattern of LH secretion in women is observed, which is presumed to result from a direct action of androgen or its conversion to estrogen. Two strategies are available to study the effect of testosterone on LH secretion. One involves the use of non-steroidal compounds that block the negative feedback actions of endogenous androgens by binding to androgen receptors; the other consists only in the administration of androgens. Following these two strategies, we first studied the pulsatile gonadotrophin secretion in hyperandrogenic women, following flutamide administration, a specific androgen receptor blocker. Flutamide treatment was followed by a decrease in LH pulse amplitude and mean LH concentrations, demonstrating that androgen receptor blockade reduces LH secretion in hyperandrogenic women. To establish the level at which the androgen effect is exerted, we further studied the acute effect of testosterone (hyperandrogenic levels) and the blockade of its receptor on LH secretion in patients with severe hypothalamic deficiency treated with pulsatile GnRH (GnRHp). LH pulse profiles were assessed under GnRHp treatment alone, during testosterone and during testosterone and flutamide administration. Testosterone increased LH secretion and LH pulse amplitude. Flutamide significantly reverted the LH increase induced by testosterone. These results strongly suggest that testosterone in the hyperandrogenic female range, may facilitate LH secretion by the pituitary, effect that is reversed by the blockade of the androgen receptor.