Responses to hemorrhagic arterial pressure reduction in different ischemic renal failure models. Renal blood flow (RBF) autoregulation has been found to be impaired in both norepinephrine (NE) and renal artery clamp (RAC) rat ischemic acute renal failure models. However, the decline in RBF at the normal lower limit of autoregulation is greater in NE-ARF. The present study was designed to determine if this difference in autoregulatory profiles has potential functional and morphologic significance. After demonstrating a fall in RBF to renal perfusion pressure reduction to 90 mm Hg that was twofold more in one week NE- than RAC-ARF (p < 0.001), separate rats of both ischemic ARF types with nearly identical levels of azotemia and glomerular filtration rate reduction and sham-ARF rats were subjected to four-hour controlled reduction in mean arterial pressure to 90 by transient phlebotomy at one week. On day 9, two days after mean arterial pressure reduction, blood urea nitrogen (BUN), serum have creatinine (SCr) and creatinine clearance (CCr) showed continued improvement in RAC-ARF, but there were significant increases in BUN (46 ± 22 to 72 ± 10 mg/dl) and SCr (1.2 ± 0.2 to 1.5 ± 0.2 mg/dl) and a decline in CCr (0.434 ± 0.127 to 0.334 ± 0.079 ml/min) in the NE-ARF group (all P < 0.02). The mean sum of scores of morphologic indices of ARF was higher in NE- than RAC-ARF kidneys of rats sacrificed on day 9 but interstitial edema was the only individual index that was worse in NE-ARF. By day 14, function the parameters had improved in both ARF groups, but BUN remained significantly higher in NE-ARF than the RAC-ARF group (P < 0.01). It is concluded that there is a distinct difference in susceptibility to recurrent injury and azotemia in NE- and RAC-ARF which is likely related to differences in maintenance phase renovascular reactivity in these two ischemic ARF models.
