Abstract- We hypothesized that nitric oxide generated by inducible nitric oxide synthase (iNOS) may contribute to the homeostatic role of this agent in hyperthyroidism and may, therefore, participate in long-term control of blood pressure (BP). The effects of chronic iNOS inhibition by oral aminoguanidine (AG) administration on BP and morphologic and renal variables in hyperthyroid rats were analyzed. Four groups (n=8 each) of male Wistar rats were used: control group and groups treated with aminoguanidine (AG, 50 mg/kg/day, via drinking water), thyroxine (T_4, 50 µg/rat/day), or aminoguanidine plus thyroxine. All treatments were maintained for three weeks. Tail systolic BP and heart rate (HR) were recorded weekly. Finally, we measured BP (mmHg) and HR in conscious rats, and morphologic, plasma, and renal variables. T₄ administration produced a small BP (125±2, p<0.05) increase versus control (115±2) rats. Aminoguanidine administration to normal rats did not modify BP (109±3) or any other hemodynamic variable. However, co-administration of T₄ and AG produced a marked increase in BP (140±3, p<0.01 vs. T₄). Pulse pressure and HR were increased in both T₄- and T₄ +AG -treated groups without differences between them. Plasma NOx (µmol/L) were increased in the T₄ group (10.02±0.15, p<0.05 vs. controls 6.1±0.10), and AG reduced this variable in T₄-treated rats (6.81±0.14, p<0.05 vs. T₄) but not in normal rats (5.78±0.20). Renal and ventricular hypertrophy and proteinuria of hyperthyroid rats were unaffected by AG treatment. In conclusion, the results of the present paper indicate that iNOS activity may counterbalance the prohypertensive effects of T₄.