This study determined whether electrical stimulation (ES) of the baroreceptor afferent fibers in the aortic depressor nerve (ADN) produces hindlimb vasodilation in pentobarbital-anesthetized rats via the release of nitric oxide (NO)-containing factors (nitrosyl factors) from NO synthase-positive lumbar sympathetic nerve terminals. ES of the ADN (1-10 Hz for 15 sec) produced frequency-dependent reductions in mean arterial blood pressure (MAP) and mesenteric (MR) and hindlimb (HLR) vascular resistances. The falls in resistance were substantially smaller in hindlimb beds in which the ipsilateral lumbar sympathetic chain was transected 7-10 days previously. The maximal falls in MR and hindquarter vascular resistance (HQR) produced by 1-10 Hz ES of the ADN were unaffected by the specific inhibitor of neuronal NO synthase, 7-nitroindazole (7-NI, 45 mg/kg iv). However, the total falls in HQR (mmHg/kHz x sec) produced by these stimuli were significantly diminished by 7-NI whereas the total falls in MR were not affected. Four successive episodes of ES at 10 Hz produced equivalent reductions in MAP, MR and HQR. The peak changes in these parameters were not affected by 7-NI. However, the total falls in HQR progressively diminished with each successive stimulus whereas the total falls in MR remained unchanged. These results provide evidence that the hindlimb vasodilation produced by ES of baroreceptor afferents within the ADN may involve the activation of post-ganglionic lumbar sympathetic vasodilator fibers which release newly synthesized and preformed nitrosyl factors.