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Effect of losartan on renal microvasculature during chronic inhibition of nitric oxide visualized by micro-CT

¹Department of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester 55905; ²Department of Biological Sciences, Minnesota State University, Mankato, Minnesota 56001; and ³Department of Physiology, Universidad de Murcia, Spain 30100

Submitted 24 March 2003 ; accepted in final form 26 June 2003

Chronic inhibition of nitric oxide (NO) synthase with the competitive L-arginine analog N^G-nitro-L-arginine methyl ester (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 ANG II AT₁ receptor antagonist losartan and L-NAME prevents the alterations in blood pressure and renal hemodynamics. Microcomputed tomography (micro-CT) was used to investigate the role of ANG II in the changes of renal microvasculature during chronic NO inhibition. Sprague-Dawley rats were given L-NAME with or without AT₁ receptor antagonist losartan (40 mg · kg^-1 · day^-1 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 three-dimensional renal images was studied using computerized analytic techniques. Kidneys of L-NAME-treated rats had significantly fewer normal glomeruli (28,824 ± 838) than those of control rats (36,266 ± 3,572). Losartan normalized the number to control values (34,094 ± 1,536). The amount of vasculature in the cortex, outer medulla, and inner medulla of L-NAME-treated rats was about two-thirds 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 AT₁ receptor blockade abolished those changes, the data suggest that the reduction in vasculature is mediated by ANG II through AT₁ receptors.

N^G-nitro-L-arginine methyl ester; angiotensin II

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