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The effects of non‐pressor and pressor doses of nitric oxide synthase inhibitor on renal excretion and regional blood flow in rat kidneys

While intrarenal administration of NO synthases inhibitors (NOSI) cause antinatriuresis, systemic infusion cause natriuresis (UNaV) which has been attributed to the associated increase in arterial pressure (AP). However, some studies show a time discrepancy between the rise in AP and UNaV. To evaluate the role of AP changes on renal function, the effects of L‐NAME (a nonselective NOSI), infused i.v., at non‐pressor (NPD, 5‐20 μg/kg/min) or pressor doses (PD, 50) were compared in anesthetized rats (n=12). UNaV was measured for 180 min together with inulin clearance (GFR) and renal cortical and medullary blood flows (CBF, MBF). The NPD increased UNaV after 150 min (0.7 ± 0.2 vs. 2.1 ± 0.4 μmol/min/g). The PD increased AP significantly after 30 min (115 ± 4 vs. 122 ± 4 mmHg), whereas UNaV increased after 60 min (1.1 ± 0.3 vs. 3.3 ± 0.7 μmol/min/g). GFR averaged 874 ± 44 μl/min/g and was not significantly altered by either NPD or PD. After 30 min of L‐NAME infusion, both NPD and PD reduced CBF and MBF. Moreover, the effects were dose related with CBF reduced by 17 ± 5% and 35 ± 6% and MBF by 27 ± 5% and 57 ± 7% for NPD and PD, respectively. Thus, NOSI effects on urinary sodium excretion effects are not directly related to changes in systemic arterial pressure and occur in presence of decreases in medullary and cortical blood flow.