Microinjection of S--amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) in the nucleus of the solitary tract (NTS) of conscious rats causes hypertension, bradycardia and vasoconstriction in the renal, mesenteric and hindquarter vascular beds. In the hindquarter, the initial vasoconstriction is followed by vasodilation with AMPA doses greater than 5 pmol/100nl. To test the hypothesis that this vasodilation is due to activation of a nitroxidergic pathway in the NTS, we examined the effect of pre-treatment with the nitric oxide synthase (NOS) inhibitor N^G-nitro-L-arginine methyl ester (L-NAME, 10 nmol/100nl, microinjected into the NTS) on changes in mean arterial pressure (MAP), heart rate (HR), and regional vascular conductance (VC) induced by microinjection of AMPA (10 pmol/100 nl in the NTS) in conscious rats. AMPA increased hindquarter VC by 18 ± 4 %, but after pre-treatment with L-NAME, AMPA reduced hindquarter VC by 16 ± 7 % and 17 ± 9 % (5 and 15 min after pre-treatment, p < 0.05 compared to before pre-treatment). Pre-treatment with L-NAME reduced AMPA-induced bradycardia from 122 ± 40 bpm to 92 ± 32 bpm, but did not alter the hypertension induced by AMPA (35±5 mmHg before pretreatment, 43±6 mmHg after pretreatment). Control injections with D-NAME did not affect resting values nor the response to AMPA. The present study shows that the stimulation of AMPA receptors in the NTS activates both vasodilatory and vasoconstrictor mechanisms, and that the vasodilator mechanism depends on production of NO in the NTS.