1. Plasma renin reactivity (PRR) is the rate of angiotensin I production after addition of renin to plasma, minus endogenous renin activity. PRR is increased in plasma of patients with renal failure compared with that of normal subjects. The present study was carried out to determine if increased PRR in uraemic plasma is related to differences of endogenous active or inactive renin, endogenous renin substrate, or pH of the incubation in vitro.
2. PRR in plasma of ten uraemic patients was greater (P<0.02) than that in plasma of ten normal subjects in incubations carried out at pH 7.4 and 5.7.
3. Increased PRR was not accounted for by differences of endogenous active and inactive renin activity.
4. After addition of renin, renin concentration (measured by direct radioimmunoassay) did not differ in normal and uraemic plasma.
5. Renin substrate concentration, measured both indirectly and by direct radioimmunoassay, also did not differ in normal and uraemic plasma.
6. Increased PRR in uraemic plasma is not related to alterations of renin or renin substrate concentrations. These observations are consistent with our earlier hypothesis that there is a deficiency of a renin inhibitor in uraemic plasma.