The role of renal nerves on renal and cardiovascular responses to adenosine administration and/or acute NO synthase inhibition was investigated. Conscious male Wistar rats with implanted catheters in femoral artery for blood pressure registration, femoral vein for drug infusion and bladder for urine collection were used. Adenosine was applied i.v. (1.0 mg/kg BW bolus) followed by infusion of 0.1 mg/kg·min, and/or nitric oxide synthase inhibition (NOSI) was performed by i.v. administration of 10 mg/kg BW N-Ω-nitro- L-arginine methyl ester (L-NAME) before and 1 week after bilateral renal denervation (BRD). NOSI decreased HR and increased SAP, MAP and DAP both in intact and BRD rats. Baroreflex sensitivity increased in intact and BRD rats. Adenosine did not change HR, blood pressure or baroreflex sensitivity in intact as well as BRD rats. NOSI increased V, VU<sub>Na</sub> and VU<sub>CI</sub> in intact rats but decreased V and did not alter VU<sub>Na</sub> and VU<sub>CI</sub> in BRD rats. Adenosine increased V, VU<sub>CI</sub> and C<sub>cr</sub> in intact rats but did not change renal excretory function in BRD rats. Combined application of adenosine and L-NAME led to a dramatic increase of V, VU<sub>Na</sub>, VU<sub>Cl</sub> and C<sub>cr</sub> in intact rats. However, VU<sub>Na</sub> and VU<sub>CI</sub> in BRD rats were lower as compared to intact rats. Therefore, changes in renal excretory function seen after NOSI are not exclusively the result of pressure diuresis and natriuresis but in some way are dependent on renal nerves. Renal denervation attenuates the renal excretory response to adenosine. Sympathetic nervous system is important in mediating the effects of adenosine and/or NO on renal excretory function. Renal denervation did not change the pattern of baroreflex sensitivity after adenosine and/or L-NAME administration.