SUPEROXIDE ACTIVITY DOES NOT PLAY A ROLE IN THE MEDIATION OF PRESSURE NATRIURESIS.

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Nitric oxide (NO) synthase inhibition enhances superoxide (O2−) activity and attenuates arterial pressure induced natriuretic responses in the kidney. To examine whether an alteration in O2− activity involved in the mediation of pressure natriuresis, we evaluated the renal responses to acute changes in renal arterial pressure (RAP), before and during intra-arterial administration NO synthase inhibitor, nitro-L-arginine (NLA, 50 μg/kg/min) followed by co-infusion of NLA and a O2− scavenger, tempol (0.5 mg/kg/min) in the denervated kidneys of 5 anesthetized sodium replete dogs. As reported earlier, NLA infusion alone decreased renal blood flow (4.9 ± 0.8 to 3.3 0.5 mL/min/g), sodium excretion (UNaV; 0.93 ± 0.16 to 0.23 ± 0.06 μmol/min/g) without an appreciable change in glomerular filtration rate (0.71 ± 0.03 to 0.67 ± 0.10 mL/min/g). UNaV responses to stepwise reductions in RAP (140 to 90 mmHg) were attenuated during NLA infusion (RAP vs UNaV slope decreased from 0.05 ± 0.002 to 0.02 ± 0.002 μmol/min/g/mmHg; P<0.003). Co-infusion of tempol with NLA increased sodium excretion (0.42 ± 0.1 μmol/min/g) but failed to reverse the attenuated slope of the relation between RAP and UNaV (0.02 ± 0.003 μmol/min/g/mmHg). These data do not indicate any involvement of intrarenal O2− activity in RAP induced changes in sodium excretion and further support a mediatory role of NO in the phenomenon of pressure natriuresis.