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1 Department of Physiology, Tulane University Health Sciences Center, New Orleans, LA, USA
* To whom correspondence should be addressed. E-mail: majid{at}tulane.edu.
To assess the role of superoxide (O2-) and nitric oxide (NO) interaction in mediating the renal actions of angiotensin II (Ang II), we examined the renal responses to intraarterial 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 prior to tempol infusion caused decreases of 24± 4% in renal blood flow (RBF), 55±7% in urine flow (V) and 53±8% in UNaV 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 UNaV; however, Ang II in the presence of tempol caused a smaller degree of decreases in RBF (-12±2%), in V (-16± 5%) and in UNaV (-27±10%) with a slight increase in GFR (6.6± 2.8%) than the responses observed prior to 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 UNaV (-11±14% vs -32±7%). These data demonstrate that renal responses to AngII are partly mediated by O2- generation and its interaction with NO. The sodium retaining effect of AngII is greatly influenced by O2- generation, particularly in the condition of NO deficiency.
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