Angiotensin converting enzyme (ACE) converts angiotensin I (AI) and also hydrolyzes bradykinin (BK), so it represents a central physiological bridge connecting these two vasoactive systems. We reported an hepatic portal hypertensive response (PHR) to BK, in contrast to its arterial vasodilation systemic effect. Previously we showed that ACE inhibitors (ACEi) prolonged BK hepatic half-life but did not alter the PHR. The effect of ACEi brings a new concept of interaction of these two systems: it has been described that ACEi resensitize the B₂ receptor (B₂R) potentiating the BK effect in cultured cell lines. Aim: to investigate the cross-talk between ACE and the B₂R in the liver. Methods: Isolated liver perfusion was performed with portal vein (afferent entry) and vena cava (efferent exit) cannulated in rats submitted or not to a chronic treatment with ACEi (enalapril at 20 mg/L added into the drinking water) for 4 weeks. Vasoactive peptides, 3.3nmol AI followed by 200nmol BK were injected; after that, the perfusion fluid was changed and BK was injected. Portal pressure was continuously monitored and the PHR was calculated (AUC: Δ portal pressure versus perfusion time) and expressed as cmH₂O.min. Liver viability was analyzed by glucose release, BSP clearance and bile production. ACE serum activity was determined using fluorogenic substrate. Results: The chronic treatment with enalapril (n=5) was effective (t test, P<0.0001) in lowering serum ACE activity (137.9±17.6 U/mL) as compared to the control group (378.9±27.6 U/mL). The hepatic viability was not altered. The capacity of the liver to convert AI to AII, demonstrated by the PHR of the generated AII was signicantly lower (P=0.0004) in the group chronically treated with enalapril (2.3±0.2 cmH₂O.min) as compared to control (21.5±3.4 cmH₂O.min). The table shows the PHR (mean ± SEM) of two successive doses of BK:

Financial support: FAPESP / CNPq