1. The effect of arachidonic acid on kallikrein release was studied in an isolated rat kidney perfused with a modified Krebs-Henseleit solution.
2. Kallikrein activity was measured in both venous and urinary effluents, after DEAE-Sephadex chromatography with D-Val-Leu-Arg-p-nitroanilide as a substrate.
3. Arachidonic acid (AA) (30 nmol/ml) induced a threefold increase in kallikrein activity in the venous effluent (control = 131 ± 9 kallikrein amidase μ-units/ml vs AA = 411 ±49 kallikrein amidase μ-units/ml, P < 0.005).
4. The stimulatory effect of arachidonic acid on kallikrein release is mediated by prostaglandins, since it can be prevented by the addition of indomethacin (1 μg/ml).
5. Our results demonstrate that kallikrein is released by the perfused kidney into the renal venous effluent, and that this release can be hormonally regulated by a mechanism involving prostaglandin synthesis.