Alleviation of anoxic experimental acute renal failure in rats by beta-adrenergic blockade.
Acute renal failure induced in Charles River rats by right nephrectomy and left renal artery clamping for 70 min, constantly produced high blood urea and serum creatinine levels 24 h following the experimental procedure. The intravascular administration of propranolol in different doses persistently alleviated the severity of uremia seen on the following day. The optimum dose in this experimental set-up was 1 mg/kg/h. The mean blood urea level was 237 +/- 15.5 (SEM) mg% in the saline-treated controls and 116 +/- 16 mg% in the group treated with propranolol 1 mg/kg/h. P113 alone and prostaglandin A1 alone were not effective in alleviating the ARF. The combination of P113 and propranolol produced the same amount of alleviation in uremia as propranolol alone. The PRA was low in the propranolol-treated rats and high in the group which received both P113 and propranolol, even though alleivation of ARF was produced in both of these groups. The mechanism by which the beta-adrenergic blockade produced by propranolol alleviates the anoxic type of acute renal failure is unknown. However, it does not seem to act through the suppression of renin release from the kidney.
D058186:Acute Kidney Injury / Q000188:drug therapy*; D000804:Angiotensin II / Q000037:antagonists & inhibitors; D000818:Animals; D004195:Disease Models, Animal; D004305:Dose-Response Relationship, Drug; D005260:Female; D009584:Nitrogen / Q000097:blood; D011433:Propranolol / Q000627:therapeutic use*; D011454:Prostaglandins A / Q000627:therapeutic use; D051381:Rats
D011454:Prostaglandins A; D000804:Angiotensin II; D011433:Propranolol; D009584:Nitrogen