Degree of renal artery stenosis alters nitric oxide regulation of renal hemodynamics.

Endothelium-derived nitric oxide (EDNO) maintains RBF in normal kidneys and to the nonclipped kidney of two-kidney, one-clip (2K, 1C) renovascular hypertensive rats. However, in clipped kidneys with severe renal stenosis, EDNO has been reported not to influence RBF, and it was suggested that low perfusion diminishes the stimulus of shear stress for EDNO synthesis. It was hypothesized that lesser degrees of renal artery stenosis would allow greater renal perfusion and, hence, a greater role for EDNO in maintaining RBF in the clipped kidney. The renal response to EDNO synthesis inhibition was studied with 10 mg/kg body wt N omega-nitro-L-arginine methyl ester (L-NAME). Four weeks after clipping, rats had different degrees of (functional) renal artery stenosis as determined by the ratio (R) of RBF (per gram kidney weight) in the nonclipped to clipped kidney. Stenosis was classified as either mild (R < or = 1.25) or moderate (R > or = 1.30). Both groups were similarly hypertensive (146 +/- 3 versus 148 +/- 6 mm Hg, respectively) and responded to L-NAME with a 42 mm Hg rise in blood pressure. In 2K,1C rats with mild renal artery stenosis, the renal response to L-NAME was similar in both nonclipped and clipped kidneys. RBF decreased by 17 to 19% (P < 0.005) and renal vascular resistance (RVR) increased by 59 to 63% (P < 0.005). When renal perfusion pressure was controlled, the decrease in RBF was exaggerated 3.6-fold in the nonclipped but only 2.3-fold in the clipped kidney, whereas the RVR increased proportionally.(ABSTRACT TRUNCATED AT 250 WORDS)