To test whether angiotensin (All) induces proteinuria via its effect on renal hemodynamics, or by another mechanism, two experimental approaches were used. In the first, it was found that All was as effective in inducing proteinuria in nephrotic as in intact rats. In all All augmented proteinurias, filtration fraction was increased. These effects plus electrophoretic profiles of All proteinuria in intact rats suggested that hemodynamic changes underly the increased glomΕrular permeability to protein. In the second approach, the All inhibitor, sar-ala-angiotensin, does not itself induce proteinuria or changes in GFR and RPF, but prevented the hemodynamic responses to All and the proteinuric response as well.