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.