[LHRH in man. Current data]

LHRH physiology is now well known. This decapeptide is released every 60 to 120 minutes by the hypothalamic pulse generator. Dopamine, noradrenaline, prostaglandins and endogenous morphinomimetics play a role in its regulation. Testosterone exerts its feed back exclusively at the hypothalamic level. LHRH action at the pituitary level is mediated through high affinity receptors. LHRH internalization is not necessary for its action which is calcium-dependent. At the testicular level, LHRH receptors are identical to those on the pituitary. Acute administration of LHRH increases both receptors on the pituitary and the testis. The synthesis of LHRH analogs with prolonged effects has produced agonist and antagonist substances which both inhibit gonadotropins. This gonadotrope inhibition is explained, in the case of agonists by both pituitary and gonadal desensitization in animal experiments. This last action is linked to LH increase. In the rat, LHRH has also led to a parallel impairment of steroidogenesis by 17 hydroxylase and 17-20 desmolase deficiency. The physiological effect of LHRH is produced exclusively by pulsatile administration. It can now be considered for the treatment of hypogonadotrophic hypogonadism. Moreover, the gonadotrope inhibition induced by LHRH agonist with prolonged action can be of therapeutic use in idiopathic precocious puberty, prostatic cancer and inhibition of spermatogenesis (an association with androgens being necessary in this last case).