Chronic inhibition of nitric oxide (NO) synthase with the competitive L-arginine analog, L-NAME, leads to an elevated systemic blood pressure and reduction in renal blood flow without significant changes in urinary sodium and water excretion. Simultaneous administration of angiotensin II AT-1 receptor antagonist losartan and L-NAME prevents the alterations in blood pressure and renal hemodynamics. Micro-computed tomography (micro-CT) was used to investigate the role of angiotensin II (AII) in the changes of renal microvasculature during chronic NO inhibition. Sprague-Dawley rats were given L-NAME with or without an AT-1 receptor antagonist, losartan (40mg/kg/d each) in their drinking water for 19 days. Kidneys from each group (control, L-NAME and L-NAME + losartan treated rats) were perfusion-fixed in situ, infused with a silicon based polymer containing lead chromate, and scanned by micro-CT. The microvasculature in the reconstructed 3-dimensional renal images was studied using computerized analytical techniques. Kidneys of L-NAME treated rats had significantly fewer normal glomeruli (28,824 ± 838) than those of control rats (36,266 ± 3572). Losartan normalized the number to control values (34,094 ± 1536). The amount of vasculature in the cortex, outer medulla and inner medulla of L-NAME treated rats was about 2/3 that of control rats; losartan normalized the values to control levels. These data indicate that chronic treatment with the NO synthase inhibitor L-NAME produces a generalized rarefaction of renal capillaries. Because simultaneous AT-1 receptor blockade abolished those changes, the data suggest that the reduction in vasculature is mediated by AII through AT-1 receptors.