Intrarenal distribution of blood flow in sodium depleted and sodium loadedrats: 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 d epletion, SD), normal (N) or high (sodium load, SL) NaCl diet. Intrarenal h emodynamics was studied in anaesthesia. NOS inhibition decreased renal bloo d flow and increased renal vascular resistance in each group, Cortical and outer medullary but not inner medullary blood flow increased in direct rati o to the sodium intake. NOS inhibition decreased the blood flow and increas ed the vascular resistance in all layers of the kidney in SID, N, and SL ra ts as well. In SID and N, but not in SL rats L-NAME induced vasoconstrictio n was higher in the outer (OM) and inner medulla (IM) than in the cortex (C ) [SD: Delta CVR 43%, Delta OMVR 54%, Delta IMVR 84%; N: Delta CVR 54%, Del ta OMVR 96%, Delta IMVR 106%; SL: Delta CVR 50%, Delta OMVR 64%, Delta IMVR 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 vas cular 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 t he dietary salt evoked vascular adaptation in the kidney. Copyright (C) 200 1 S. Karger AG, Basel.