Nitric oxidc is continuously released in the circulation where it can quickly modify the hemodynamic conditions and therefore affect blood pressure variability. Nevertheless the effect of nitric oxide on blood pressure variability has not been completely elucidated; moreover it remains unknown whether nitric oxide acts independently, in concert or in opposition with the autonomic nervous system. In order to answer these questions we studied the effects of nitric oxide synthesis inhibition in intact, sympathectomized (Sympx) and sino-aortic denervated (SAD) conscious WKY rats. Mean arterial pressure (MAP) and pulse interval (PI) were continuously recorded for 60 minutes both in absence and in presence of an 1-arginine analogue, 1-NMMA (iv bolus 100 mg.kg^-1, followed by a 1.5 mg.kg^-1 .min^-1 infusion for 60 minutes). Data were analyzed by means of FFT power spectral analysis in the HF (3.0 to 0.8 Hz), MF (0.6 to 0.1 Hz), and LF (0.1 to 0.025 Hz) frequency bands. Sympathectomy moderately reduced MAP whereas SAD did not change it significantly. 1-NMMA increased MAP (intact: from 97.2±3.6 to 135.4±4.2 mmHg, p<0.01; Sympx: from 73.6±3.9 to 124.3±5.9 mmHg, p<0.01; SAD: from 101.0±14.5 to 141.1±19.4 mmHg, p<0.01). Spectral analysis of both MAP and PI showed a different effect of 1-NMMA in the three groups of rats: 1-NMMA reduced significantly MF power of MAP in intact rats (from 1.67±0.60 to 0.75± 0.24 mmHg² p<0.001) and in SAD rats (from 2.90±0.80 to 1.86±0.90, p <0.05) but not in sympathectomized rats (from 0.67±0.37 to 0.60±0.32 mmHg², p=ns). Concerning PI, 1-NMMA increased significantly LF power in sympathectomized rats and HF power in both intact and sympathectomized rats (all p<0.01) but it did not modify spectral powers in SAD rats. In conclusion our data suggest that 1) nitric oxide contributes to generate overall blood pressure variability in the mid frequency range and 2) this effect is related to an interaction between nitric oxide and sympathetic neural influences.