Intrarenal Distribution of Blood Flow in Sodium Depleted and Sodium Loaded Rats: Role of Nitric Oxide

The renal hemodynamic effects of nitric oxide synthase (NOS) inhibition and dietary salt were studied in rats. L-NAME (0.1 mg/ml in the drinking fluid, about 12 mg/kg/day) was given for 4 days to rats receiving low (sodium depletion, SD), normal (N) or high (sodium load, SL) NaCl diet. Intrarenal hemodynamics was studied in anaesthesia. NOS inhibition decreased renal blood flow and increased renal vascular resistance in each group. Cortical and outer medullary but not inner medullary blood flow increased in direct ratio to the sodium intake. NOS inhibition decreased the blood flow and increased the vascular resistance in all layers of the kidney in SD, N, and SL rats as well. In SD and N, but not in SL rats L-NAME induced vasoconstriction was higher in the outer (OM) and inner medulla (IM) than in the cortex (C) [SD: ΔCVR 43%, ΔOMVR 54%, ΔIMVR 84%; N: ΔCVR 54%, ΔOMVR 96%, ΔIMVR 106%; SL: ΔCVR 50%, ΔOMVR 64%, ΔIMVR 35%]; in normal rats blood flow shifts from the medulla toward the cortex. In conclusion, nitric oxide may have a role in the regulation of renal vascular tone not only in the case of regular sodium uptake but in the sodium depleted or loaded organism as well. However, nitric oxide has no role in the dietary salt evoked vascular adaptation in the kidney.