17b-estradiol and prolactin inhibit nitric oxide pathway in anterior pituitary cells in culture from adult, ovariectomized rats

CABILLA JP, RONCHETTI SA, NUDLER SI, MILER EA, QUINTEROS AF, DUVILANSKI BH

Rio de Janeiro, Brasil

Congreso; 13th International Congress of Endocrinology; 2008

Nitric oxide (NO) is a freely diffusive molecule that acts as a second messenger in a variety of cellular processes. It is synthesized by constitutive (NOS-1 and NOS-3) and inducible NO (NOS-2) synthases, and exerts its effects mainly through its intracellular receptor, soluble guanylyl cyclase (sGC). Several evidence sustain that NO may act in both the brain and anterior pituitary (AP) as a neuroendocrine regulator of reproductive function. NOS-1 is present mainly in gonadotrophs and follicle-stellate cells in AP. It was previously reported that after gonadectomy, NOS levels and hence NO production are augmented in pituitary gland. Pituitary NOS-1 is negatively regulated by gonadal steroids via modulation of GnRH secretion. Results from our lab show that E2 directly down-regulates NO pathway by modifying sGC expression and by decreasing its activity in AP. Besides, we have demonstrated that NO inhibits prolactin (PRL) release from AP and E2 modifies the sensitivity of AP to its inhibitory action, thus suggesting the existence of an interplay between both pathways.