Amelioration with vessel dilator of acute tubular necrosis and renal failure established for 2 days

Seventeen Sprague-Dawley rats had ischemic nonoliguric acute renal failure (ARF) induced by vascular clamping resulting in their preischemic blood ure a nitrogen (BUN) and creatinine levels of 16 +/- 1 and 0.56 +/- 0.05 mg/dl to increase to 162 +/- 4 and 8.17 +/- 0.5 mg/dl, P < 0.001, respectively, a t day 4 of postischemia. Vessel dilator, a 37-amino-acid cardiac peptide ho rmone (0.3 mu g.kg(-1)min(-1) ip), decreased the BUN and creatinine levels to 53 +/- 17 mg/dl and 0.98 +/- 0.12 mg/dl; (P < 0.001) in another seven an imals where ARF had been established for 2 days. Water excretion doubled wi th ARF and was further augmented by vessel dilator. Transthoracic echocardi ography revealed left ventricular dilation as a probable cause of the incre ase in vessel dilator in the circulation with ARF, and vessel dilator infus ion reversed this dilation. At day 6 of ARF, mortality decreased to 14% wit h vessel dilator from 88% without vessel dilator Acute tubular necrosis was <5% in the vessel dilator-treated rats compared with 25% to >75% in the pl acebo-treated ARF animals. We conclude that vessel dilator improves acute t ubular necrosis and renal function in established ARF.