We have shown that inhibition of nitric oxide syntase (NOS) increases hormonal secretion of vasopressin (VP) and oxytocin (OT) and that nitric oxide (NO) donor reduces plasma concentrations of VP and OT in response to central stimulation of angiotensin-II (ANGII). In the present study we analyzed in hypothalamic paraventricular (PVN) and supra-optic (SON) nuclei the time course effect of central ANGII stimulation on mRNA expression of VP, OT and NOS by Real Time PCR. We also evaluated the influence of NO donor or inhibitor in these mRNA expressions. Wistar male rats (n=5-6), anaesthetized with 2.5% tribromoethanol (1ml/100g bw, ip) with a stainless cannula placed into the right lateral ventricle were injected with ANGII (50ng) and 30, 60, 90, 120 and 240 min later, the animals were decapitated and the PVN and SON nuclei microdissected. Another group of rats received, 20 min before ANGII, a central pretreatment with NOS inhibitor (Nw-Nitro-L-arginine methyl ester, LNAME 250µg) or NO donor (S-Nitroso-N-acetylpenicillamine, SNAP 5µg) and PVN and SON were collected 60 min after ANGII stimulation. The results are reported as means±SEM and the data were analyzed by t student test (signif. P<0.05). Values obtained from control animals were 1.0±0.2 arbitrary units (au). ANGII induced an increase in VP mRNA expression in both PVN and SON at 30, 60, 90 and 120 min after stimulation (peak at 60min: PVN 2.7±0.3, SON 2.2±0.1 au). An increase in OT mRNA expression was observed only at 30 and 60 min after ANGII (peak at 60min: PVN 2.2±0.3, SON 1.9±0.2 au). NOS expression after ANGII stimulation was increased at 30 and 60 min in the PVN and at all experimental periods in the SON (peak at 60min: PVN 1.6±0.1, SON 2.1±0.2 au). Therefore, the highest VP, OT and NOS mRNA expression induced by central ANGII occurred at 60 min after the stimulation. Animals submitted to injection of LNAME alone showed an increase in VP (PVN 2.4±0.2, SON 1.9±0.2 au) and OT (PVN 2.4±0.1, SON 2.1±0.3 au) mRNA expression, but a slightly reduction in NOS expression (PVN 0.8±0.1, SON 0.8±0.1 au). Pretreatment with LNAME did not change ANGII induced VP and OT expression, but it reduced NOS mRNA expression (PVN 1.1±0.1, SON 1.1±0.1 au). In ANGII stimulated rats, pretreatment with SNAP decreased the VP (PVN 1.7±0.1, SON 1.4±0.1 au) and OT (PVN 1.5±0.1, SON 1.5±0.1 au) mRNA expression, without effects on NOS expression. In conclusion, collectively with our previous results, the present data indicate that central angiotensinergic system facilitates VP, OT and NOS expression and NO reduces VP and OT expression responses to ANGII, suggesting an inhibitory modulation of NO in the control of neurohypophysial hormones synthesis and release.