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1 Physiology, Tulane University Health Sciences Center, New Orleans, LA, USA
* To whom correspondence should be addressed. E-mail: majid{at}tulane.edu.
To evaluate the role of a potential interaction between superoxide anion (O2-) and nitric oxide (NO) in regulating the kidney function, we examined the renal responses to intraarterial infusion of a superoxide dismutase mimetic, tempol (0.5 mg.kg-1.min-1) in anesthetized dogs treated with or without NO synthase inhibitor, nitro-L-arginine (NLA; 50 :g.kg-1.min-1). In one group of dogs (n=10), tempol infusion alone for 30 min prior to 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 :L.min-1.g-1) or sodium excretion (UNaV; 2.4±0.3 to 2.2±0.3 :mol.min-1.g-1). Interestingly, when tempol was infused in another group dogs (n=12) pretreated with NLA, it caused increases in V (4.4 ± 0.4 to 9.7 ±1.4 :L.min-1.g-1) and in UNaV (0.7 ± 0.1 to 1.3±0.2 :mol.min-1.g-1) without affecting RBF or GFR. Although NO inhibition caused usual qualitative responses in both groups of dogs, the anti-diuretic (47 ± 5% vs 26 ± 4%) and anti-natriuretic (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 co-administration 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.
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