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Oxidative Stress

Inhibition of nitric oxide synthase enhances superoxide activity in canine kidney

Department of Physiology, Tulane University Health Sciences Center, New Orleans, Louisiana 70112

Submitted 2 February 2004 ; accepted in final form 24 March 2004

To evaluate the role of a potential interaction between superoxide anion (O₂^–) and nitric oxide (NO) in regulating kidney function, we examined the renal responses to intra-arterial infusion of a superoxide dismutase mimetic, tempol (0.5 mg·kg^–1·min^–1), in anesthetized dogs treated with or without NO synthase inhibitor, N-nitro-L-arginine (NLA; 50 µg·kg^–1·min^–1). In one group of dogs (n = 10), tempol infusion alone for 30 min before NLA infusion did not cause any significant changes in renal blood flow (RBF; 5.2 ± 0.4 to 5.0 ± 0.4 ml·min^–1·g^–1), glomerular filtration rate (GFR; 0.79 ± 0.04 to 0.77 ± 0.04 ml·min^–1·g^–1), urine flow (V; 13.6 ± 2.1 to 13.9 ± 2.5 µl·min^–1·g^–1), or sodium excretion (U_NaV; 2.4 ± 0.3 to 2.2 ± 0.3 µmol·min^–1·g^–1). Interestingly, when tempol was infused in another group of dogs (n = 12) pretreated with NLA, it caused increases in V (4.4 ± 0.4 to 9.7 ± 1.4 µl·min^–1·g^–1) and in U_NaV (0.7 ± 0.1 to 1.3 ± 0.2 µmol·min^–1·g^–1) without affecting RBF or GFR. Although NO inhibition caused usual qualitative responses in both groups of dogs, the antidiuretic (47 ± 5 vs. 26 ± 4%) and antinatriuretic (67 ± 4 vs. 45 ± 11%) responses to NLA were seen much less in dogs pretreated with tempol. NLA infusion alone increased urinary excretion of 8-isoprostane (13.9 ± 2.7 to 22.8 ± 3.6 pg·min^–1·g^–1; n = 7), which returned to the control levels (11.6 ± 3.4 pg·min^–1·g^–1) during coadministration of tempol. These data suggest that NO synthase inhibition causes enhancement of endogenous O₂^– levels and support the hypothesis that NO plays a protective role against the actions of O₂^– in the kidney.

renal hemodynamics; sodium excretion; superoxide dismutase mimetic; tempol; N-nitro-L-arginine

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