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1. Acute renal failure was produced in rats by the intramuscular injection of glycerol (6.1 mol/l 10 ml/kg). Either 2 or 4--6 h later the right kidney was isolated and perfused for 1 h with an electrolyte solution containing a gelatin preparation (Haemaccel, 35 g/l) at pressures between 90 and 100 mm Hg in a single-pass system. 2. In kidneys taken from rats with acute renal failure renal vascular resistance was markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly impaired after 1 h of perfusion and fractional reabsorption of sodium and water as well as the secretion of p-aminohippurate were diminished. Renal venous renin concentration and renin release were lower in kidneys taken from rats with acute renal failure than in the control experiments. 4. These results suggest that the increase in renal vascular resistance and the stimulation of renin release after injection of glycerol in vivo are the consequence of extra- rather than intra-renal mechanisms.

1. In rats deprived of food and water for 24 h acute renal failure was produced by the intramuscular injection of glycerol. Eight hours later plasma urea concentration had increased threefold despite a small rise in urine volume. Plasma concentrations of renin and renin substrate were elevated. 2. When saralasin, a competitive antagonist of angiotensin II, was infused for 8 h after glycerol injection, urine volume and plasma urea were similar to values in rats that had received an infusion of saline. 3. Administration of rat serum (4.5 ml h-1 kg-1) for 4 h suppressed plasma renin concentrations, but plasma urea increased to the same extent as in rats without serum. 4. When saralasin and serum were infused at the same time, urine volume, urine osmolality and solute excretion increased and the rise of plasma urea was diminished. 5. Saralasin has a protective effect against glycerol-induced acute renal failure only when volume is replaced concomitantly.

1. During the development of glycerol-induced acute renal failure in Sprague-Dawley rats, plasma concentrations of vasopressin rise and probably induce an increase in blood pressure. 2.In the present studies the role of vasopressin in acute renal failure was further analysed by experiments in Brattleboro rats homozygous for hereditary hypothalamic diabetes insipidus which were injected intramuscularly with 10 ml of glycerol/kg (6 1 mmoV1).3. After the injection of glycerol plasma osmolality increased transiently and packed cell volume was elevated. The rats became anuric and plasma urea concentrations rose progressively. Plasma renin concentration increased significantly within 2 h. Plasma renin substrate concentration rose progressively and had almost doubled by 8 h.4. In contrast with previous observations in Sprague-Dawley rats, blood pressure did not rise in rats with diabetes insipidus after the injection of glycerol.5. When 2 h after the injection of glycerol kidneys were taken from rats with diabetes insipidus and perfused with an electrolyte solution in a single-pass system for 1 h, renal vascular resistance was 30% higher than in control kidneys 10 min after the start of the perfusion and remained elevated thereafter. In similar experiments with kidneys from Sprague-Dawley rats with acute renal failure, renal vascular resistance was increased fivefold immediately after the start of the perfusion, but decreased subsequently.6. These data support the idea that in glycerolinduced acute renal failure of Sprague-Dawley rats an increased release of vasopressin is responsible for the elevation of blood pressure and suggest that this hormone also participates in renal vasoconstriction. However, a rise of plasma vasopressin concentrations alone cannot fully explain the increase in renal vascular resistance and the development of acute renal failure.

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