BENEFICIAL EFFECT OF PROPRANOLOL IN A HISTOLOGICALLY APPROPRIATE MODEL OF POSTISCHEMIC ACUTE RENAL-FAILURE

  • 1 January 1977
    • journal article
    • research article
    • Vol. 88  (1) , 163-+
Abstract
Acute renal failure caused in the rabbit by clamping one renal pedicle for 1 h and removing the opposite kidney produced a histologic picture very similar to that observed in hypotensive acute renal failure in man. I.v. infusion of propranolol, a drug which prevents renin release, at 1 mg/kg for 70 min beginning at time of pedicle clamping resulted in significantly lower serum creatinine in this model (2.8 .+-. 0.2 mg% at 48 h with propranolol vs. 5.2 .+-. 0.8 mg% without). Renin stimulation by dehydration or feeding a low-salt diet enhanced the difference between treated and untreated groups (2.6 .+-. 0.4 mg% with propranolol vs. 6.2 .+-. 1.8 mg% without, after dehydration; 3.5 .+-. 1.0 mg% with propranolol vs. 7.6 .+-. 1.4 mg% without, after low-salt diet). Suppression of renin production by saline feeding eliminated propranolol''s beneficial effect (5.6 .+-. 0.9 mg% with propranolol vs. 4.0 .+-. 0.6 mg% without). In rabbits with a normal food and water intake, renal denervation using phenol also eliminated propranolol''s effect (creatinine 8.6 .+-. 1.4 mg% with propranolol vs. 8.6 .+-. 1.8 mg% without). In rabbits with intact kidneys, flow probe recording of renal blood flow showed a significantly higher blood flow immediately after unclamping in the propranolol-treated animals, and renal angiograms showed less vasoconstriction in this group after unclamping. In this model of acute renal failure, renal vasoconstriction plays an important role following the initial ischemic insult. Propranolol lessens the severity of this vasoconstriction and the resulting acute renal failure. Its probable action is interference with neurogenically stimulated renin release.