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Superoxide scavenging attenuates renal responses to ANG II during nitric oxide synthase inhibition in anesthetized dogs

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

Submitted 9 August 2004 ; accepted in final form 4 October 2004

To assess the role of superoxide (O₂^–) and nitric oxide (NO) interaction in mediating the renal actions of ANG II, we examined the renal responses to intra-arterial infusion of ANG II (0.5 ng·kg^–1·min^–1) before and during administration of a superoxide dismutase mimetic, tempol (0.5 mg·kg^–1·min^–1), in the presence or absence of NO synthase inhibitor, nitro-L-arginine (NLA; 50 µg·kg^–1·min^–1), in anesthetized dogs pretreated with enalaprilat (33 µg·kg^–1·min^–1). In one group of dogs (n = 7), ANG II infusion before tempol infusion caused decreases of 24 ± 4% in renal blood flow (RBF), 55 ± 7% in urine flow (V), and 53 ± 8% in urinary sodium excretion (U_NaV) with a slight decrease in glomerular filtration rate (GFR; –7.8 ± 3.4%). Tempol infusion alone did not cause significant alterations in RBF, GFR, V, or U_NaV; however, ANG II in the presence of tempol caused a smaller degree of decreases in RBF (–12 ± 2%), in V (–16 ± 5%), and in U_NaV (–27 ± 10%) with a slight increase in GFR (6.6 ± 2.8%) than the responses observed before tempol. In another group of NLA-treated dogs (n = 6), tempol infusion also caused significant attenuation in the ANG II-induced responses on RBF (–13 ± 3% vs. –22 ± 7%), GFR (–19 ± 5% vs. –33 ± 3), V (–15 ± 12% vs. –28 ± 4%), and U_NaV (–11 ± 14% vs. –32 ± 7%). These data demonstrate that renal responses to ANG II are partly mediated by O₂^– generation and its interaction with NO. The sodium-retaining effect of ANG II is greatly influenced by O₂^– generation, particularly in the condition of NO deficiency.

renal hemodynamics; sodium excretion; tempol; nitro-L-arginine

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