Effect of nitric oxide synthase inhibition on renal circulation and excretory function in anaesthetized rats

The effects of nitric oxide synthase (NOS) inhibition (effected using L-NAM E, 14 mg (kg body mass (BM))(-1) administered intravenously) on systemic an d renal circulation and renal excretory function has been investigated in a naesthetized Wistar rats subjected to one of two different degrees of isoto nic extracellular (EC) volume expansion (40 and 60 ml kg(-1) (240 min)(-1)) . The administration of L-NAME resulted in an increase in mean arterial blo od pressure and total peripheral vascular resistance (TPR), and a significa nt reduction in cardiac output (CO) and the kidney Fraction of CO in both e xperimental groups. The total renal blood flow (RBF) dropped from 557 +/- 4 3.4 to 149 +/- 13.1 ml min(-1) (100 g BM)(-1) and from 592 +/- 45.9 to 191 +/- 16.3 ml min(-1) (100 g BM)(-1) in the 40 and 60 ml kg(-1) (240 min)(-1) experimental volume expansion groups, respectively. A redistribution of th e intrarenal circulation from the medulla of the kidney toward the cortex m ay have occurred. The NOS inhibition induced a significant decrease in the glomerular filtration rate (GFR; from 1.18 +/- 0.10 to 0.53 +/- 0.08 ml min (-1) (100 g BM)(-1) and from 1.26 +/- 0.07 to 0.73 +/- 0.08 ml min(-1) (100 g BM)(-1) in the 40 and 60 ml kg(-1) (240 min)(-1) experimental volume exp ansion groups, respectively), and the filtration fraction increased. The ur ine excretion dropped in parallel with the GFR, while the reduction in sodi um and potassium excretion was more marked than that of the GFR, raising th e possibility of a direct effect on the kidney tubules. The difference in E C volume expansion (the calculated increases in the EC volume in the last 9 0 min were 1.30 and 5.44% in the two time control groups and 3.66 and 7.45% in the two L-NAME-treated groups) did not induce any significant modificat ion of the L-NAME effect.