1. Acute renal failure was produced in rats by intramuscular injection of glycerol. Subsequently, changes in the concentrations of renin and of angiotensin II in plasma and the renin content of the kidneys were followed. 2. At 4 and 8 h after glycerol administration, plasma renin and angiotensin II had increased two-to three-fold; they remained elevated for 48 h and then returned towards normal. At 7 days, the values were still slightly raised. 3. At 4 and 8 h after glycerol injection, kidney renin had decreased but it had increased after 24 and 48 h. 4. Passive immunization with angiotensin II antibodies, given at the time of glycerol injection and 2 and 4 h afterwards, prevented the development of acute renal failure. When angiotensin II antiserum was administered later (8, 10 and 12 h after glycerol) it had no effect. 5. Stimulation of the renin-angiotensin system may be involved in the pathogenesis of the early phase of acute renal failure.
1. Antibodies against angiotensin II were purified by affinity chromatography. 2. When injected intravenously into rats, the antibody distributed in the extracellular space with a half-time of 11 h and a distribution volume of about 10 ml/100 g body weight. The antibody was eliminated with a half-time of 7 days. 3. Plasma angiotensin II concentrations increased about 100-fold the control values 7 min after antibody injection and declined in parallel with the antibody concentration. It was calculated that only about 1–4% of the binding capacity of the antibody was occupied by angiotensin throughout the experiment. 4. Since the plasma renin concentration was normal, except during the short initial phase of stimulation, it is concluded that upon antibody injection the renin-angiotensin system rapidly, reached an equilibrium, with concentrations of free angiotensin close to or identical with normal concentrations.