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Failure of Chronic Sodium Chloride Loading to Protect against Norepinephrine‐Induced Acute Renal Failure in Dogs

We previously have shown that chronic sodium chloride (NaCI) loading protects against HgCI2-induced acute renal failure (ARF) in dogs. To determine whether NaCI loading protects against an ischemic model of ARF, unilateral oliguric renal failure was produced by the infusion of norepinephrine (NE) into the renal artery of both saline-expanded (SE) and water-drinking (WD) dogs (n = 7). The renal renin content (30 U/g kidney) of SE dogs was suppressed (P < 0.001) compared to that of WD dogs (132 ± 18). Forty-eight hours after infusion of NE (1.5 fig/kg per min x 100 min), inulin clearances from the infused kidney of SE (6 ml/min ± 2) and WD dogs (7 ± 2) did not differ; in both groups, respective clearances from the noninfused kidney (43 ml/min ± 3) and (36 ± 5) also did not differ from each other. The percent fall in renal blood flow to the infused kidney 48 hours after NE in SE (44%) and WD dogs (38%) did not differ. Because of failure to demonstrate protection, a lower dose of NE (0.75μg/kg Per m +- n x 40 min) was infused into SE and WD animals (n = 6). Forty-eight hours after low dose NE, inulin clearances of the infused kidney of SE (17 ml/min ± 5) and WD dogs (17 ± 4) did not differ. Respective clearances in the noninfused kidney of SE (46 ml/min ± 6) and WD dogs (35 ± 4) did not differ. Therefore, despite suppression of renal renin content, NaCI loading failed to protect against this ischemic model of ARF. In conclusion, unlike HgCI2-induced ARF, it is unlikely that the renin angiotensin system contributes to the pathogenesis of this ischemic model of ARF.