We have shown previously, that a moderate reflex increase in renal sympathetic nerve activity (RSNA) elevated glomerular capillary pressure, while a more severe increase in RSNA decreased glomerular capillary pressure. This suggested that the nerves innervating the glomerular afferent and efferent arterioles could be selectively activated allowing differential control of glomerular capillary pressure. A caveat to this conclusion was that intrarenal actions of neurally stimulated ANGII might have contributed to the increase in post-glomerular resistance. This has now been investigated. Anaesthetised rabbits were prepared for renal micropuncture and RSNA recording. One group (ANGII clamp) received an infusion of an angiotensin converting enzyme inhibitor (enalaprilat; 2 mg/kg bolus plus 2mg/kg/h) plus ANGII (~20 ng/kg/min), the other vehicle. Measurements were made before (room air) and during 14%O₂. Renal blood flow decreased less during ANGII clamp compared to vehicle (9±1 % vs 20±4 %, P_GT<0.05), despite a similar increase in RSNA in response to 14%O₂ in the two groups. Arterial pressure and glomerular filtration rate were unaffected by 14%O₂ in both groups. Glomerular capillary pressure increased from 33±1 to 37±1 mmHg during ANGII clamp and from 33±2 to 35±1 mmHg in the vehicle group before and during 14%O₂, respectively (P_GT<0.05). During ANGII clamp, post-glomerular vascular resistance was still increased in response to RSNA during 14%O₂, demonstrating that the action of the renal nerves on the post-glomerular vasculature was independent of the renin-angiotensin system. Further supporting our hypothesis that increases in RSNA can selectively control pre- and post-glomerular vascular resistance and therefore glomerular ultrafiltration.