The endothelial cell should be regarded as a highly active metabolic and endocrine organ interacting with the blood streak and the interstitium. Kinins are vasodepressor hormones that may participate in local blood flow regulation as part of an autocrine-paracrine system. We have previously reported that tissue kallikrein, its mRNA and kininogen are present in vascular tissue. The present study was undertaken to examine the release of the components of this system from isolated perfused rat vessels. These vessels were perfused at 4 ml/min with physiological saline solution containing 3% Ficoll and 0.1% BSA. Kallikrein was released into the perfusate at a rate of 75 +/- 5 ng Bk/100 g bw/30 min (n = 10). Kininogen was released at a rate of 55 +/- 5 pg Bk/100 g bw/30 min. Pre-treatment with puromycin, a protein synthesis inhibitor, significantly reduces kallikrein and kininogen release. Vascular derived kinins were released at a constant rate of 38 +/- 6 pg Bk/100 g bw/30 min for at least 120 min. This basal kinin release was increased 3-fold when perfused with the angiotensin converting enzyme inhibitor ramiprilat (p < 0.05). When purified kininogen was added to the physiological saline solution, immunoreactive kinins in the perfusate increased from 42 +/- 7 to 3140 +/- 210 pg Bk/100 g bw/30 min (n = 6; p < 0.002). Increase in flow rate (from 2 ml/min up to 4 ml/min and 8 ml/min) causes a parallel increase in the release of kinins (from 32 +/- 4 up to 48 +/- 6 and 62 +/- 8 pg Bk/100 g bw/30 min, respectively; p < 0.01); the increase may be due to the effect of shear stress upon the endothelial cells. The present data confirm that vascular tissue synthesizes and releases continuously kallikrein, kininogen and kinins. Vascular kinins induce potent vasodilatation through the release of prostacyclin, nitric oxide and endothelium-derived hyperpolarization factor, and some of the converting enzyme inhibitors effect may be explained by potentiation of vascular-derived kinins.