In chloralose-anesthetized dogs, we investigated the disappearance of bradykinin on passage across the renal circulation. The peptide was infused into a renal artery at various doses (5-200 ng/kg min~'); renal blood flow and the concentration of kinins in renal venous blood were then determined and the percent survival of bradykinin on passage through the kidney calculated. Bradykinin caused a dose-related increase in renal blood flow, urine flow, sodium excretion, and kinin content of renal

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... ous blood. Intravenous administration of BPP 9cr (300 /ig/kg), a peptide kininase II inhibitor, potentiated the renal vasodilator, diuretic, and natriuretic actions of bradykinin and augmented the survival of the kinin on passage through the kidney from 12.72 ± 1.64% in control dogs to 53.92 ± 7.48% (P < 0.001). Furthermore, the values of peptide survival were positively correlated with the increases in renal blood flow (r = 0.92, P < 0.01), urine flow (r = 0.75, P < 0.01), and sodium excretion (r = 0.68, P < 0.01) produced by bradykinin. In addition, BPP 9a by itself increased renal blood flow (16%, P < 0.01), urine flow (115%, P < 0.005), and sodium excretion (167%, P < 0.02). Similarly, the concentration of kinin in renal venous blood and the excretion of urinary kinins rose from 0.11 ± 0.03 ng/ml and 4.4 ± 1.1 ng/min to 0.24 ± 0.05 ng/ml (P < 0.005) and 38.5 ± 12.2 ng/min (P < 0.02). These studies suggest that kinins generated intrarenally play a role in the regulation of renal blood flow and salt-water excretion and that variations in the capacity of the kidney to inactivate kinins may be a determinant of the intrarenal activity of the kallikrein-kinin system.