Nitric oxide dependence of renal blood flow in patients with renal artery stenosis

In ischemia, nitric oxide (NO) production is increased, possibly to preserv e flow. The role of NO was investigated in hypertensive patients with or wi thout renal artery stenosis (RAS). Fifty-five hypertensive patients schedul ed to undergo diagnostic renal angiography underwent mean renal blood flow (MRBF) measurements before and after an intrarenal injection of the NO synt hase blocker N-g-monomethyl-L-arginine (L-NMMA) at 0.03 mug/kg, before angi ography. A dose-response study indicated that this dose Of L-NMMA significa ntly blocked NO synthesis. MRBF was measured at baseline and 1, 5, 10. and 20 min after L-NMMA treatment. On the basis of the angiographic results, pa tients were divided into three diagnostic categories, i.e., essential hyper tension (n=26), unilateral RAS (n=16), or bilateral RAS (n=8). In essential hypertension, MRBF was decreased by 18 +/-4% at 20 min. In unilateral RAS, L-NMMA did not affect MRBF in the stenotic kidney but reduced MRBF in the nonstenotic kidney by 40 +/-9% at 20 min. In bilateral RAS, L-NMMA reduced flow by 32 +/- 14% at 20 min. In the nonstenotic kidney in unilateral RAS. a positive correlation was observed between the effect of NO blockade on MR BF and arterial renin levels (P=0.009). In the stenotic kidney, in contrast , this correlation was inverse (P=0.007). In conclusion, MRBF depends on NO in hypertensive patients. except in the stenotic kidney in unilateral RAS. In the nonstenotic kidney in unilateral RAS, NO bioavailability is increas ed. It is suggested that a compensatory mechanism, regulated by NO and poss ibly angiotensin II, may preserve renal function.