Renal nitric oxide and angiotensin II interaction in renovascular hypertension.

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Abstract
In two-kidney, one clip (2K1C) renovascular hypertension, blood flow is reduced to the clipped but not to the nonclipped kidney, despite elevated angiotensin II. To determine possible interactions between endothelium-derived nitric oxide and angiotensin, we studied bilateral renal blood flow using radioactive microspheres in anesthetized 2K1C hypertensive rats 4 weeks after clipping. We studied the response to nitric oxide synthesis inhibition with 10 mg/kg body wt NG-nitro-L-arginine- methyl ester (L-NAME) in hypertensive rats untreated (n = 5) or treated (n = 5) with 10 mg/kg body wt of the angiotensin II antagonist losartan. 2K1C rats had a blood pressure of 159 +/- 9 mm Hg, and renal blood flow to the clipped kidney was reduced 87% compared with the nonclipped kidney. L-NAME increased blood pressure 36 +/- 5 mm Hg and decreased renal blood flow in the nonclipped kidney 61% (4.9 +/- 0.5 to 1.9 +/- 0.4 mL/min per gram kidney weight, P < .001). Renal vascular resistance increased 200% (33.4 +/- 2.2 to 100.7 +/- 15.0 resistance units [RU], P < .005). Renal blood flow and resistance in the clipped kidney were unchanged by L-NAME. Treatment of 2K1C rats with losartan reduced blood pressure (154 +/- 8 to 116 +/- 11 mm Hg, P < .01), did not change blood flow in the nonclipped, but normalized it in the clipped kidney (4.8 +/- 0.8 mL/min per gram kidney weight).(ABSTRACT TRUNCATED AT 250 WORDS)