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Rat kidneys were perfused with an artificial solution at constant pressure. The infusion of angiotensin II (AII) (1.5--6 ng min-1) reduced renal perfusate flow (RPF) from 36.6 +/- 2.4 to 19.3 +/- 1.4 ml min-1 (P less than 0.001) (n = 13); GFR rose from 0.48 +/- 0.06 to 0.63 +/- 0.04 ml min-1 (P less than 0.05), and filtration fraction (FF) rose accordingly from 0.015 +/- 0.002 to 0.033 +/- 0.003 (P greater than 0.01). The same results were obtained with purified renin substrate (synthetic tetradecapeptide, 100 ng min-1, n = 8); RPF fell from 31.5 +/- 2.9 to 17.2 +/- 2 ml min-1 (P less than 0.001), GFR rose from 0.36 +/- 0.05 to 0.51 +/- 0.04 ml min-1 (P less than 0.05), and FF increased from 0.021 +/- 0.002 to 0.034 +/- 0.006 (P less than 0.01). The effects of renin substrate were completely prevented by the converting enzyme inhibitor SQ 20,881 (3 X 10(-5) M). In another six experiments the effects of renin substrate at the same dose were fully reversed by addition of the analogue [Sar1,Ala8]AII. We interpret these findings to indicate that both exogenous and endogenous AII produce preferential vasoconstriction of the efferent arteriole, increasing the driving force for ultrafiltration and thereby maintaining or increasing GFR in the face of a reduced plasma flow.

The local, direct effect of endogenous angiotensin II (AII) in the isolated, perfused rat kidney was studied in an "open-circuit," single-pass preparation perfused at a constant pressure with an artificial solution containing 6.5% bovine albumin in Krebs-Ringer solution. After the addition of purified renin substrate (tetradecapeptide, 3 to 5 X 10(-8) M), renal plasma flow fell from 25.3 +/- 1.6 to 14.4 +/- 1.0 ml x min-1 (N = 6, P < 0.001) and GFR rose from 0.3 +/- 0.03 to 0.63 +/- 0.06 ml.min-1 (P < 0.001). Filtration fraction rose accordingly from 0.015 +/- 0.001 to 0.044 +/- 0.002 (P < 0.001). The effects of the renin substrate were promptly reversed by the addition of an angiotensin antagonist, Sar1-Al8-AII (3 X 10(-6) M). Measurements of distribution of perfusate flow between outer and inner cortex were made with radioactive microspheres. Outer cortical flow was 75.3 +/- 3.5% of the total cortical flow during the control periods and 73.7 +/- 2.3% during the maximal renin substrate effect. We conclude that endogenous AII is active locally, independent of systemic recirculation. Its major site of action in this preparation is on the efferent glomerular arteriole.

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