1. Renin release from the isolated perfused rat kidney was markedly stimulated by isoprenaline or anoxia. Renin secreted into the blood-free perfusate was not activated by exposure to cold or dialysis to pH 3·3, suggesting the absence either of cryo- or acid-activatable renin or of factors necessary to activate inactive renin.
2. Trypsin treatment did not change renin concentration in the perfusate samples.
3. When binephrectomized rat plasma was added to perfusate samples before dialysis, renin concentration in the acidified samples was significantly higher than in samples dialysed to pH 6·5. Diminished renin recovery in the latter samples caused this difference. Binephrectomized rat plasma itself had no significant renin activity before or after acid dialysis, indicating the absence of any important extrarenal source of active or acid-activatable renin in rats.
4. Acidification of binephrectomized rat plasma before its addition to the perfusate samples markedly reduced the difference between renin recovery during dialysis to pH 3·3 and dialysis to pH 6·5, indicating that acidification irreversibly inhibited renin inactivation by binephrectomized rat plasma. No net increase in renin concentration was observed in any of our experiments.
5. These results suggest that rat kidney does not secrete inactive renin. They also point to the existence of renin inactivation by rat plasma at neutral pH, which might lead to overestimation of acid-activatable renin in rats.