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Chronic two-kidney, one clip (2K1C) renovascular hypertension is characterized by a largely angiotensin-independent elevated blood pressure (BP). We hypothesized that the long-term effect of hypertension would compromise endothelium-derived nitric oxide (NO) and diminish its influence in controlling renal perfusion. We determined the influence of endothelium-derived NO on renal hemodynamics and the angiotensin-NO interaction regulation of renal perfusion in rats with chronic 2K1C hypertension. Renal blood flow (RBF) was measured by radioactive microspheres in rats with either early-phase (4 weeks after clipping, n=7) or chronic-phase (13 to 16 weeks after clipping, n=7) 2K1C hypertension. The systemic and renal response to NO synthesis inhibition was determined with 10 mg/kg body wt N omega-nitro-L-arginine methyl ester (L-NAME). In rats with early-phase 2K1C hypertension, BP was 149+/-3 mm Hg, which increased by 42+/-3 mm Hg with L-NAME (P&lt;.001). L-NAME decreased RBF by 20% (P&lt;.02) and 17% (P&lt;.005) and increased renal vascular resistance (RVR) by 58% (P&lt;.005) and 62% (P&lt;.02) in the nonclipped and clipped kidneys, respectively. In rats with chronic 2K1C hypertension, BP was 166+/-3 mm Hg, and L-NAME increased this by 35+/-6 mm Hg (P&lt;.001). In the nonclipped and clipped kidneys of chronic 2K1C hypertensive rats, L-NAME decreased RBF by 20% (P&lt;.01) and 17% (P&lt;.01) and increased RVR by 51% (P&lt;.005) and 60% (P&lt;.02), respectively. There were no differences in L-NAME-induced changes between early- and chronic-phase 2K1C hypertensive rats. Next, we treated seven chronic-phase 2K1C hypertensive rats with 10 mg/kg body wt losartan, which reduced BP by only 7.7% (P&lt;.005). After losartan, L-NAME increased BP by 41+/-3 mm Hg (P&lt;.001), decreased RBF to the nonclipped kidney by 44% (P&lt;.05), and increased RVR by 110% (P&lt;.005); the decrease in RBF was significantly greater compared with untreated chronic-phase controls (P&lt;.05). In the clipped kidney, L-NAME decreased RBF by 26% (P&lt;.05) and increased RVR by 76% (P &lt;.05). Thus, angiotensin blockade did not attenuate the systemic or renal vasoconstriction to L-NAME. Our results suggest that in both early and chronic phases of 2K1C hypertension, NO contributes significant dilator tone to buffer the hypertension and maintains perfusion of both kidneys by counterbalancing angiotensin-independent vasoconstriction.

Influence of Nitric Oxide in the Chronic Phase of Two-Kidney, One Clip Renovascular Hypertension